Spine: Rehabilitation Medicine Quick Reference Series

Spine Rehabilitation Medicine Quick Reference Ralph M. Buschbacher, MD Series Editor Professor, Department of Physica...

Author: Andre Panagos | MD

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Spine

Rehabilitation Medicine Quick Reference Ralph M. Buschbacher, MD Series Editor Professor, Department of Physical Medicine and Rehabilitation Indiana University School of Medicine Indianapolis, Indiana

n Spine André Panagos

n Spinal Cord Injury Thomas N. Bryce

Forthcoming Volumes in the Series Traumatic Brain Injury Musculoskeletal, Sports, and Occupational Medicine Pediatrics Neuromuscular/EMG Prosthetics Stroke

Spine Rehabilitation Medicine Quick Reference

André Panagos, MD Department of Rehabilitation Medicine New York-Presbyterian Hospital Weill Cornell Medical Center New York, New York

New York

Acquisitions Editor: Beth Barry Cover Design: Steve Pisano Compositor: NewGen North America Printer: Bang Printing Visit our website at www.demosmedpub.com © 2010 Demos Medical Publishing, LLC. All rights reserved. This book is protected by copyright. No part of it may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without the prior written permission of the publisher. Medicine is an ever-changing science. Research and clinical experience are continually expanding our knowledge, in particular our understanding of proper treatment and drug therapy. The authors, editors, and publisher have made every effort to ensure that all information in this book is in accordance with the state of knowledge at the time of production of the book. Nevertheless, the authors, editors, and publisher are not responsible for errors or omissions or for any consequences from application of the information in this book and make no warranty, express or implied, with respect to the contents of the publication. Every reader should examine carefully the package inserts accompanying each drug and should carefully check whether the dosage schedules mentioned therein or the contraindications stated by the manufacturer differ from the statements made in this book. Such examination is particularly important with drugs that are either rarely used or have been newly released on the market.

Library of Congress Cataloging-in-Publication Data Panagos, Andre. Spine / Andre Panagos. p. ; cm.—(Rehabilitation medicine quick reference) Includes bibliographical references and index. ISBN 978–1–933864–28–0 (alk. paper) 1. Spine—Diseases—Handbooks, manuals, etc. I. Title. II. Series: Rehabilitation medicine quick reference. [DNLM: 1. Spinal Diseases—Handbooks. 2. Spine—physiopathology—Handbooks. WE 39 P187s 2009] RD768.P26 2009 616.7⬘3—dc22 2009022795

Special discounts on bulk quantities of Demos Medical Publishing books are available to corporations, professional associations, pharmaceutical companies, health care organizations, and other qualifying groups. For details, please contact: Special Sales Department Demos Medical Publishing 11 West 42nd Street, 15th Floor New York, NY 10036 Phone: 800-532-8663 or 212-683-0072 Fax: 212-941-7842 Email: [email protected] Made in the United States of America 09 10 11 12

5 4 3 2 1

To my wife, Sophia, whose love and unwavering support enriched each page, and to our daughter, Marilia, who blessed us with her birth during this project.

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Contents

List of Acronyms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . x Series Foreword . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .xi Preface . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xiii

Conditions of the Spine 1. Achondroplasia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2 2. Aging Lumbosacral Spine . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4 3. Aneurysmal Bone Cysts . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6 4. Ankylosing Spondylitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8 5. Anterior Cord Syndrome (Anterior Spinal Artery Syndrome) . . . . . . . . . . . . . . 10 6. Arachnoiditis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12 7. Arteriovenous Malformation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14 8. Atlantoaxial Instability . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16 9. Aviation-Associated Back and Neck Pain . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18 10. Baastrup’s Disease (Kissing Spines Disease) . . . . . . . . . . . . . . . . . . . . . . . . . 20 11. Back Pain Associated with Dance . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22 12. Back Pain Associated with Golf . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24 13. Back Pain Associated with Heavy Loads. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26 14. Back Pain Associated with Occupation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28 15. Back Pain Associated with Pregnancy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30 16. Back Pain Associated with Sitting . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 32 17. Back Pain Associated with Soccer . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 34 18. Back Pain Associated with Tennis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 36 19. Back Pain in Mature Athletes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38 20. Back Pain in the Older Population . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 40 21. Back Pain in Young Athletes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 42 22. Brown-Séquard Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 44 23. Cauda Equina Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 46 24. Central Cord Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 48 25. Chondrosarcoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 50 26. Chordoma. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 52 27. Coccydynia (Coccygodynia) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 54 28. Deconditioning . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 56 29. Diffuse Idiopathic Skeletal Hyperostosis (Forrestier’s Disease) . . . . . . . . . . . 58

vii

viii

Contents

30. Disciitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 60 31. Ehlers–Danlos Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 62 32. Epidural Abscess . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 64 33. Epidural Lipomatosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 66 34. Ewing’s Sarcoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 68 35. Failed Back Surgery Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 70 36. Fractures, Lower Cervical Spine . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 72 37. Fractures, Upper Cervical Spine . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 74 38. Fractures, Sacrum . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 76 39. Fractures, Thoracolumbar Spine . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 78 40. Giant Cell Tumor . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 80 41. Hemangiomas . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 82 42. Hemoglobinopathies (Sickle Cell Disease, Thalassemia) . . . . . . . . . . . . . . . . 84 43. Hyperparathyroidism . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 86 44. Low Back Strain . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 88 45. Lymphoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 90 46. Marfan Syndrome. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 92 47. Meningioma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 94 48. Meningitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 96 49. Multiple Myeloma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 98 50. Multiple Sclerosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 100 51. Myofascial Pain Syndrome. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 102 52. Neck Pain Associated with Occupation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 104 53. Neck Pain in Athletes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 106 54. Neck Strain . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 108 55. Neurofibroma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 110 56. Osteoblastoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 112 57. Osteochondroma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 114 58. Osteogenesis Imperfecta . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 116 59. Osteoid Osteoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 118 60. Osteomyelitis, Vertebral Body . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 120 61. Osteoporosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 122 62. Paget’s Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 124 63. Psoriatic Arthritis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 126 64. Radiculopathy, Cervical . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 128 65. Radiculopathy, Lumbar . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 130 66. Radiculopathy, Thoracic. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 132

Contents

67. Rheumatoid Arthritis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 134 68. Sacroiliac Joint Pain . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 136 69. Sarcoidosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 138 70. Scheuermann’s Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 140 71. Schwannoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 142 72. Scoliosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 144 73. Spinal Cord Injury . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 146 74. Spinal Stenosis, Cervical (Cervical Myelopathy) . . . . . . . . . . . . . . . . . . . . . 148 75. Spinal Stenosis, Lumbar . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 150 76. Spinal Stenosis, Thoracic (Thoracic Myelopathy) . . . . . . . . . . . . . . . . . . . . 152 77. Spondylolysis/Spondylolisthesis, Cervical . . . . . . . . . . . . . . . . . . . . . . . . . 154 78. Spondylolysis/Spondylolisthesis, Lumbar . . . . . . . . . . . . . . . . . . . . . . . . . . 156 79. Spontaneous Epidural Hematoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 158 80. Stingers and Burners . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 160 81. Synovial Cysts . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 162 82. Syringomyelia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 164 83. Tarlov Cysts (Perineural Cysts, Sacral Nerve Root Cysts) . . . . . . . . . . . . . . 166 84. Tethered Cord Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 168 85. Transverse Myelitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 170 86. Whiplash-Associated Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 172 87. Zygapophyseal (Facet) Joint Pain, Cervical . . . . . . . . . . . . . . . . . . . . . . . . . 174 88. Zygapophyseal (Facet) Joint Pain, Lumbar . . . . . . . . . . . . . . . . . . . . . . . . . 176

Spine-Mimicking Conditions 89. Carpal Tunnel Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 180 90. Complex Regional Pain Syndrome (Reflex Sympathetic Dystrophy) . . . . . . 182 91. Fibromyalgia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 184 92. Herpes Zoster . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 186 93. Hip–Spine Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 188 94. Lyme Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 190 95. Peripheral Neuropathy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 192 96. Piriformis Syndrome (Pseudosciatica) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 194 97. Polymyalgia Rheumatica . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 196 98. Psychological/Psychiatric Issues . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 198 99. Shoulder Impingement Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 200 100. Trochanteric Bursitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 202

Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 205

ix

List of Acronyms

CSF CT MRI NSAID PET RA SCI SPECT

x

cerebrospinal fluid computed tomography magnetic resonance imaging nonsteroidal anti-inflammatory drugs positron emission tomography rheumatoid arthritis spinal cord injury single-photon emission computed tomography

Series Foreword

The Rehabilitation Medicine Quick Reference (RMQR) series is dedicated to the busy clinician. While we all strive to keep up with the latest medical knowledge, there are many times when things come up in our daily practices that we need to look up. Even more importantly . . . look up quickly. Those aren’t the times to do a complete literature search or to read a detailed chapter or review article. We just need to get a quick grasp of a topic that we may not see routinely, or just to refresh our memory. Sometimes a subject comes up that is outside our usual scope of practice, but that may still impact our care. It is for such moments that this series has been created. Whether you need to quickly look up what a Tarlov cyst is, or you need to read about a neurorehabilitation complication or treatment, RMQR has you covered. RMQR is designed to include the most common problems found in a busy practice, but also a lot of the less common ones as well. I was extremely lucky to have been able to assemble an absolutely fantastic group of editors. They in turn have

harnessed an excellent set of authors. So what we have in this series is, I hope and believe, a tremendous reference set to be used often in daily clinical practice. As series editor, I have of course been privy to these books before actual publication. I can tell you that I have already started to rely on them in my clinic—often. They have helped me become more efficient in practice. Each chapter is organized into succinct facts, presented in a bullet point style. The chapters are set up in the same way throughout all of the volumes in the series, so once you get used to the format, it is incredibly easy to look things up. And while the focus of the RMQR series is, of course, rehabilitation medicine, the clinical applications are much broader. I hope that each reader grows to appreciate the Rehabilitation Medicine Quick Reference series as much as I have. I congratulate a fine group of editors and authors on creating readable and useful texts. Ralph M. Buschbacher, MD

xi


Preface

This book was conceived as a quick reference guide for the most common spine disorders. It was born out of my frustration in finding relevant research articles to help in evaluating and treating complex patients that I saw in our spine center. For many conditions, relevant information was difficult to find and the law of parsimony was of limited value. This text is broken down into the 100 most common spine disorders, with each topic presented in a clear and consistent two-page format. There were a larger number of etiologies that I uncovered, but in many cases there was little scientific literature available. Finding research literature on the conditions that I did include was also sometimes challenging. I also took the liberty to include a section on common spine-mimicking conditions as they are sometimes indistinguishable from true spine disorders.

This book would not have been possible had it not been for my mentors in physical medicine and rehabilitation who provided the mandate and led the way in spine care: Stanley Herring, MD, Stuart Kahn, MD, and Willibald Nagler, MD. I would also like to acknowledge Michael W. O’Dell, MD, who supported my intellectual motivation to tackle this project; and acknowledge my collegues, Roger Hartl, MD, Keith Hentel, MD, Matthew Lipp, MD, and Tracy Maltz, DPT, who always challenge me with new and interesting cases. Finally, I would like to thank our residents and visiting medical students who were courageous enough to ask the questions that only raw curiosity puts forth. There were, of course, triumphs and failures as I compiled the “Top 100” and I hope that through my frustration I have improved your outcomes in the battlefield of spine care. André Panagos, MD

xiii


Spine


I

Conditions of the Spine

Achondroplasia Description

n

Achondroplasia is the most common form of dwarfism, resulting in a characteristically large head with frontal bossing and a long narrow trunk with short limbs.

Diagnosis

Etiology/Types n n n

Autosomal-dominant inheritance Fibroblast growth factor receptor 3 (FGFR3) gene point mutation causes 95% of cases. 80% of cases are new mutations.

Epidemiology n n n

Achondroplasia is the most common form of dwarfism. Occurs in 1 in 10,000 to 30,000 live births Affects 250,000 individuals worldwide

Pathogenesis n

Decreased endochondral bone growth

Risk Factors n n

Familial inheritance Spontaneous mutation risk factors are unknown.

80% of affected individuals have neurogenic claudication by 60 years of age.

Differential diagnosis Hypochondroplasia n Severe achondroplasia with developmental delay and acanthosis nigricans n Thanatophoric dysplasia types I and II n

History Increasing neck or low back pain n Increased weakness n Decreased function and mobility n

Exam Short stature n Large head with frontal bossing n Hypoplastic midface n Long narrow trunk with short limbs n Lower motor neuron or upper motor neuron findings n Fixed kyphoscoliosis or exaggerated lumbar lordosis n

Clinical Features n n n n n n n n n n n

Large head with frontal bossing Hypoplastic midface Long narrow trunk with short limbs Joint hyperextensibility affecting the hands and knees Restricted elbow rotation and extension Thoracolumbar gibbus may develop by 4 months of age leading to a fixed kyphoscoliosis. Exaggerated lumbar lordosis Infants may develop respiratory distress due to cervical medullary compression. Motor development may be delayed due to narrowing of the foramen magnum. Tibial bowing affects 42% of the population. Neurogenic claudication and spinal stenosis are common in older children and adults.

Natural History n n n

2

Cervical and lumbar spinal stenosis with aging Increasing back pain due to spinal stenosis, exaggerated lumbar lordosis, and spondylosis 10% of affected individuals have neurogenic claudication by 10 years of age.

Anterioposterior pelvis plain radiograph demonstrating narrowed and relatively higher iliac wings and flattened acetabulae with short femoral necks. (Courtesy of Keith Hentel, MD.)

Achondroplasia

Pitfalls Repetitive nerve compression injuries may result in irreversible muscle atrophy and loss of mobility.

n

Red flags n n

Tetraplegia Cauda equina syndrome

Treatment Medical n Nonsteroidal anti-inflammatory drugs (NSAIDs) n A trial of bracing may be helpful for back pain and curvature reduction. Exercises n General strengthening and stretching Modalities n Heat, cold, ultrasound, and transcutaneous electrical nerve stimulation have been used for symptomatic relief of pain and muscle spasms. Injection Trigger point injections for symptoms of myofascial pain

n

n

Epidural steroid injection for radicular symptoms

Surgical 5% to 10% of patients have cervical medullary decompression surgery as early as infancy. n Extensive decompressive laminectomy may need to be performed, which may involve the entire spine. n Reoperation may be required within 8 years. n

Consults n Physical medicine and rehabilitation n Neurologic or orthopedic-spine surgery n Neurology Complications of treatment n Syringomyelia n Tetraplegia n Persistent and severe sciatica n Cauda equina syndrome

Prognosis n

Continued function is possible if assessed early and surgically treated.

Helpful Hints n

Repetitive nerve compression injuries may result in irreversible muscle atrophy and loss of mobility, so early treatment is important.

Suggested Readings Horton WA, Hall JG, Hecht JT. Achondroplasia. Lancet. 2007;370(9582):162–172. Siebens AA, Hungerford DS, Kirby NA. Achondroplasia: effectiveness of an orthosis in reducing deformity of the spine. Arch Phys Med Rehabil. 1987;68(6):384–388.

Section I: Conditions of the Spine

Testing n DNA testing n X-rays demonstrate normal height and width of vertebral bodies with short, thickened pedicles throughout the spine. n Narrowed central spinal canal n Exaggerated lumbar lordosis n Computed tomography (CT) is used to assess for medullary compression due to craniocervical stenosis. n Somatosensory evoked potentials (SSEP) may be used to assess cervical cord compression. n Electrodiagnostic studies to assess radicular symptoms

3

Aging Lumbosacral Spine Description

Risk Factors

With aging, the initial intervertebral disc degeneration is followed by progressive deterioration of the adjacent bone, muscles, zygapophyseal (facet) joints, and ligaments.

n


Difficult to differentiate normal aging from pathologic processes Genetic inheritance accounts for 50% to 70% of disc degeneration variability. High or repetitive mechanical loading and smoking are thought to play a role.

Epidemiology n n

Universal Progression varies widely.

Pathogenesis n n n n n

n n

n

n n n

n

4

The anterior column carries 75% of the total axial compressive load. The intervertebral disc can withstand 2.8 to 13.0 kN of compressive force. Intradiscal proteoglycan content progressively declines with advancing age. Vertebral endplate permeability decreases beginning in the second decade of life. Changes first affect the endplate, followed by the nucleus pulposus and the annulus fibrosis over several spinal levels. Calcified nucleus pulposus herniation through the endplate is called a Schmorl’s node. Degeneration of the normally avascular intervertebral disc allows blood vessels and nociceptive fibers to penetrate the disc, introducing inflammatory mediators into the previously avascular space. The degenerative cascade describes the loss of hydrostatic pressure within the nucleus pulposus, resulting in increased compressive loads on the annulus fibrosis and zygapophyseal (facet) joints. Intervertebral disc injuries never fully heal. Osteophytes increase the load-bearing surface area. The aging ligamentum flavum loses elastin content, causing anterior bulging that can contribute to central spinal stenosis. Loss of dorsal extensor muscle and the abdominal flexors muscle equilibrium

n n

Genetic inheritance High or repetitive mechanical loading Smoking

Clinical Features n n n

Ranges from painless progression to severe back pain Progressive weakness Loss of flexibility


Narrowing in adult intervertebral discs occurs at a rate of 3% per year. The majority of acute disc herniations occur between the ages of 30 and 50. 90% of lumbar discs demonstrate degeneration by the fifth decade of life.

Diagnosis Differential diagnosis Fracture n Infection n Neoplasm n Stenosis n

History Deep dull lumbosacral ache n Radiation into the buttock or posterior thighs n Morning stiffness n

Exam Lumbosacral paraspinal tenderness n Pelvic girdle muscle atrophy n

Testing X-rays demonstrate degenerative changes in 90% of patients. n Magnetic resonance imaging (MRI) can identify disc degeneration in 35% of healthy volunteers. n Larger disc herniations seen on initial imaging correspond with greater resolution of the herniation in 2 years. n No correlation with pain and disc signal intensity on MRI n

Pitfalls Overinterpretation of imaging findings

n

Aging Lumbosacral Spine n n

5

Flexion or extension bias in stretching and strengthening Mechanical evaluation to determine a direction of preference

Modalities n Heat, cold, ultrasound, and transcutaneous electrical nerve stimulation have been used for symptomatic relief of pain and muscle spasms. Injection Trigger point injections for symptoms of myofascial pain n Epidural steroid injections for symptoms related to radiculitis, radiculopathy, or stenosis Surgical n Decompression n Fusion for unrelenting pain Sagittal lumbar T2-weighted magnetic resonance image demonstrating multilevel disc degeneration that is often associated with aging.

Red Flags n n n n

Fracture Infection Neoplasm Neurologic dysfunction

Treatment

Consults n Physical medicine and rehabilitation n Neurologic or orthopedic-spine surgery Complications of treatment n Progressive pain and dysfunction even with appropriate treatment

Prognosis n

Highly variable

Helpful Hints n

Disc degeneration is an irreversible process in which intact tissue is unable to respond to progressive structural failures.

Medical n NSAIDs n Analgesics n Acupuncture has been described as helpful.

Suggested Readings

Exercises n Lumbar stabilization focuses on stabilizing the painful pathologic region with muscular development and movement patterns.

Benoist M. Natural history of the aging spine. Eur Spine J. 2003;12(Suppl 2):S86–S89. Kirkaldy-Willis WH, Wedge JH, Yong-Hing K, Reilly J. Pathology and pathogenesis of lumbar spondylosis and stenosis. Spine. 1978;3(4):319–328.


n

Aneurysmal Bone Cysts Description

n

Aneurysmal bone cysts are benign cystic hyperemic/ hemorrhagic lesions.

n

Etiology/Types Thought to be caused by trauma, which allows blood to pool within the bone, resulting in increased intraosseous pressure followed by resorption and cyst formation.

Epidemiology n n n n n n

Represents 1% or 2% of all primary bone lesions Represents 15% of all primary spine tumors 10% to 30% occur in the spine, and the remainder occur in the long bones. Primarily occurs in young adults who are under 30 years of age. 50% of patients are pediatric. Females slightly more affected than males

Pathogenesis n n

n

Cystic structure with vascular channels of unclotted blood May contain immature bony trabeculae, fibrous connective tissue, osteoid, multinucleated giant cells, and granulation tissue. Most commonly found in the posterior elements followed by the vertebral body.

n

Giant cell tumor Infection Metastasis

History Acute localized pain and swelling

n

Exam Tenderness to local palpation n Associated muscle spasm n Decreased range of motion n Kyphosis or scoliosis n

Testing X-rays demonstrate a solitary osteolytic lesion with a subperiosteal shell of bone. n MRI can delineate soft tissue expansion and detect a fluid level on T2-weighted sequences. n CT scan may show multiple-fluid levels with a thin rim of bone. n Biopsy n

Pitfalls Sacral lesions are associated with increased pathologic fractures, and a higher recurrence rate.

n

Red Flags n n n

Cauda equina syndrome Neuropathy Paraplegia

Risk Factors n

Trauma


Acute localized pain and swelling Duration of pain may be from months to several years. Severity is associated with location and may include sensory changes, paraplegia, neuropathy, or cauda equina syndrome.

Natural History n n

Pain for several months to years Increased risk for pathologic bone fractures

Diagnosis Differential diagnosis Chondroblastoma

n

6

Treatment Medical Analgesics

n

Exercises None

n

Modalities None

n

Injection None

n

Surgical Preoperative arterial embolization n En bloc resection is the preferred treatment, as there is no risk of local recurrence. n Posterior element involvement may be treated with resection and bone graft. n

Aneurysmal Bone Cysts n n

Radiotherapy is preferred for large lesions. Cryosurgery may halt expansion and prevent recurrence.

Consults Neurologic or orthopedic-spine surgery n Radiation oncology n

Complications of treatment n High intraoperative and postoperative morbidity

n n

7

The maximum rate of local recurrence is one year Irradiated patients should be followed for a lifetime due to the small risk of malignant transformation.

Helpful Hints n

Early diagnosis and treatment leads to a good prognosis and minimal morbidity.

Prognosis n n n

Commonly recur after curettage Early detection and treatment allows for an improved prognosis The location of the tumor affects the prognosis

Boriani S, De Iure F, Campanacci L, et al. Aneurysmal bone cyst of the mobile spine: report on 41 cases. Spine. 2001;26(1):27–35. Papagelopoulos PJ, Currier BL, Shaughnessy WJ, et al. Aneurysmal bone cyst of the spine. Management and outcome. Spine. 1998;23(5):621–628.


Suggested Readings

Ankylosing Spondylitis Description

n

Ankylosing spondylitis is a chronic inflammatory disease that involves the joints of the axial spine and the sacroiliac joint.

n n n n

Etiology/Types n

Unknown

Epidemiology n n n

Prevalence between 0.1% and 1.4% Male to female ratio of 2:1 Most common in males 15 to 40 years of age

Pathogenesis n

Thought to be caused by infection, trauma, or heredity

Risk Factors n n

HLA-B27 association A positive family history increases the risk up to 30% in HLA-B27–positive first-degree relatives.

n

Herniated intervertebral disc Infection Osteoarthritis Other spondyloarthropathies Rheumatoid arthritis Tumor

History Lumbosacral back pain n Subjective feeling of “stiffness” n Lower extremity radiation n Neck stiffness or pain n Peripheral joint pain n

Exam Decreased lumbosacral range of motion can be assessed using distance from fingers to the floor or Schober’s test. n Sacroiliac joint provocative maneuvers include FABER, Gaenslen, and Yoeman tests. n Flattening of the lumbar spine with loss of lumbar lordosis n Rigid gait n

Clinical Features n n n n n

n

Lower back pain is worse in the morning or with inactivity and improves with exercise. Lumbosacral back pain occurs in 81% of patients. Pseudosciatica due to piriformis muscle spasm and sciatic nerve compression Neck stiffness, pain, or torticollis 13% of patients develop peripheral joint involvement, acute iridocyclitis, plantar fascial enthesis, or Achilles tendonitis. 30% of patients may have involvement of the shoulders, elbows, hips, knees, and ankles.


n

Osteoproliferation Bone and cartilage interface chondritis or osteitis Vertebral body erosion due to inflammatory granulation tissue resulting in ankylosis of the joints and ossification of the surrounding ligaments (syndesmophytes) Progressive stiffness

Diagnosis Differential diagnosis Fibromyalgia

n

8

Lateral lumbar plain radiograph in ankylosing spondylitis demonstrating ossification of the anterior longitudinal ligament (arrow) also known as a “bamboo spine.” (Adapted from Fast A, Goldsher D. Navigating the Adult Spine: Bridging Clinical Practice and Neuroradiology. New York: Demos Medical Publishing, 2007:80.)

Ankylosing Spondylitis

Pitfalls Delayed diagnosis

n

Red Flags n n n n

Acute iridocyclitis Cauda equina syndrome Spinal instability Spondylodiscitis

Treatment Medical n Patient education n Hard mattress with no pillows for sleeping n NSAIDs for use in mild to more advanced disease n Intravenous steroids n Disease modifying antirheumatic medications for peripheral joint involvement Exercises Proper posture n Structured exercise programs have minimal evidence supporting their effectiveness, although they are commonly used. n Physical therapy should not be too aggressive. n Strengthening of the extensors of the hip, shoulder, and spine

n n

Unsupervised exercise for 30 minutes per day, 5 days per week General cardiovascular conditioning

Modalities Heat, cold, ultrasound, and transcutaneous electrical nerve stimulation have been used for symptomatic relief of pain and muscle spasms.

n

Injection None

n

Surgical Fusion for spinal instability n Total joint replacements n

Consults n Physical medicine and rehabilitation n Neurologic or orthopedic-spine surgery for spinal deformities n Ophthalmology n Cardiology for aortic incompetence and conduction deficits n Pulmonary for fibrotic changes Complications of treatment Osteoporosis n Spondylodiscitis n

Prognosis n n

Most patients remain functional and employed. Worse prognosis with younger age at onset, peripheral joint disease, elevated ESR, and poor response to NSAIDs.

n

Helpful Hints n

Pain relief and maintenance of function are the primary treatment goals.

Suggested Reading Braun J, Sieper J. Ankylosing spondylitis. Lancet. 2007;369(9570):1379–1390.


Testing n 90% of patients are positive for HLA-B27. n 80% of patients with active disease have an elevated erythrocyte sedimentation rate (ESR). n X-rays demonstrate bony changes in the sacroiliac joints and loss of the normal lumbar concave surface referred to as a “squared” look. n Extensive syndesmophyte formation referred to as “bamboo spine” n MRI localizes early spondylitic changes and contrast enhancement detects early inflammatory lesions within the lumbar spine and sacroiliac joints.

9

Anterior Cord Syndrome (Anterior Spinal Artery Syndrome) Description

n

Anterior cord syndrome is a spinal cord injury characterized by lower extremity paresis or paralysis, loss of pain and temperature sensation below the level of the lesion with preservation of vibratory sense, proprioception, light touch and two-point discrimination.

n

Etiology/Types

n

n

n

Caused by an occlusion of the anterior spinal artery, which supplies blood to the anterior horn and anterior portion of the lateral columns at each level Most commonly due to traumatic or ischemic injury to the artery of Adamkiewicz

n

Hypoxemia Retroperitoneal dissection Thoracic epidural anesthesia

Clinical Features n

n n n n

Symptom onset can be rapid, from 2 minutes to several hours. Intractable back pain at level of spinal cord ischemia Spinothalamic sensory deficits (loss of pain and temperature sensation) Preservation of light touch Bowel and bladder dysfunction Possible respiratory failure

Epidemiology n

Comprises 2.7% of all traumatic spinal cord injuries

Pathogenesis n

n

n

n n

The spinal cord is supplied by one anterior and two posterior spinal arteries, which are supplied by radicular arteries that enter the canal through the intervertebral foramen. Central arteries originate off of the anterior spinal artery supplying the anterior horn and anterior portion of the lateral columns at each level. The pial plexus surrounding the spinal cord also interconnects the anterior and posterior spinal arteries. The C1 to T3 region is perfused by the vertebral arteries at the C3 level and the cervical ascending arteries at the C6–C7 level. The T3 to T7 region is perfused by an intercostal artery at the T7 level. The T8 to the conus medullaris region is perfused from a branch of the intercostal artery (artery of Adamkiewicz) located between the T9 and T12 levels.

Natural History n

Rapid development of symptoms, from 2 minutes to several hours

Diagnosis Differential diagnosis Epidural abscess n Epidural hematoma n

History Intractable back pain at the level of spinal cord ischemia n Bowel and bladder dysfunction n Motor and sensory deficits n

Exam Loss of pain and temperature sensation n Lower extremity paresis or paralysis n

Testing MRI notes increased T2-weighted signal at the region of the ischemic lesion.

n

Pitfalls Can occur during surgery, allowing the condition to go unnoticed while the patient is anesthetized.

n

Risk Factors n n n n

Aortic surgery Arterial emboli Atherosclerotic narrowing Coronary artery bypass graft surgery

10

Red Flags n n n

Intractable pain Lower extremity paresis or paralysis Bowel and bladder dysfunction

Anterior Cord Syndrome n n

11

Household and community mobility training Activities of daily living training

Modalities n Heat, cold, ultrasound, and transcutaneous electrical nerve stimulation have been used for symptomatic relief of pain and muscle spasms. Injection None

n

Consults n Physical medicine and rehabilitation n Neurology

Sagittal thoracic T2-weighted magnetic resonance image demonstrating increased heterogeneous cord signal (arrow), compared to the upper cord that resulted in anterior cord syndrome. (Adapted from Fast A, Goldsher D. Navigating the Adult Spine: Bridging Clinical Practice and Neuroradiology. New York: Demos Medical Publishing, 2007:127.)

Treatment Medical n Vasopressors spare the cerebral and spinal vasculature Exercises n Strengthening and stretching

Complications of treatment n Neuropathic pain n Continued spinal cord injury–related issues

Prognosis n n n

Back pain may resolve within days. Long-term prognosis is determined by the sparing of the conus medullaris. 88% of patients have been successfully discharged home after inpatient rehabilitation.

Helpful Hints n

Often no identifiable cause can be found.

Suggested Reading Baba H, Tomita K, Kawagishi T, Imura S. Anterior spinal artery syndrome. Int Orthop. 1993;17(6):353–356.


Surgical n None

Arachnoiditis Description

n

Arachnoiditis is an inflammatory process resulting in fibrosis of the arachnoid membrane causing adherence and entrapment of the adjacent nerve roots.

n

Etiology/Types n n

Progressive inflammatory reaction Possible genetic component resulting in a fibrinolytic defect

Epidemiology n

Affects up to 11% of failed back surgery syndrome patients

Pathogenesis n

n n

Following injury, phagocytes and fibrolytic enzymes that usually break down fibrous bands are washed away by the cerebrospinal fluid (CSF). Fibrocytes invade the fibrous bands and lay down collagen-forming adhesions around the nerve roots. Eventual encapsulation of the nerve roots over several years results in hypoxia and progressive atrophy.

Pachymeningitis hypertrophica Spinal cord tumor

History Burning sensation in the sacral region n Severe pain down the back of the legs n Nonsciatic-type pain n Burning at the medial knees n Pain and tingling in the feet n Mobility may be severely restricted n

Exam Paraspinal tenderness n Positive straight leg raise n Muscle atrophy n Muscle spasm n Decreased ankle reflexes n Extremity weakness n

Testing n MRI demonstrates adherent nerve roots located centrally in the thecal sac, adherence of the nerve roots to

Risk Factors n n n n n n n n

Infection Intrathecal depomedrol Intrathecal hemorrhage Intrathecal medications or anesthetic agents Oil- or water-based intrathecal contrast agents Retained surgical debris or foreign bodies Spinal trauma Surgery


Very variable Constant neck or back pain Pain worsened with activity Radicular symptoms Bladder dysfunction

Natural History n n

Constant pain with limited function Symptoms usually do not progress.

Diagnosis Differential diagnosis Cauda equina syndrome 12

n

Axial lumbar computed tomography myelography demonstrating nerve root clumping (arrow) that is characteristic of arachnoiditis. (Adapted from Fast A, Goldsher D. Navigating the Adult Spine: Bridging Clinical Practice and Neuroradiology. New York: Demos Medical Publishing, 2007:140.)

Arachnoiditis

n

Pitfalls n None

Red Flags n

Progressive cauda equina syndrome

Treatment Medical Opioids for pain control n Medications for neuropathic pain n

Exercises n Exercise may be difficult due to pain n Important to encourage as much physical activity as possible Modalities n Heat, cold, ultrasound, and transcutaneous electrical nerve stimulation have been used for symptomatic relief of pain and muscle spasms. Injection n Experimental use of intrathecal hyaluronidase n Removal of residual oil-based contrast dye n Epidural steroid injection for radicular symptoms n Endoscopic lysis of adhesions Surgical Gentle handling of the neural elements during surgery can decrease the risk of development of adhesions.

n

n n

Spinal cord stimulation has demonstrated up to a 50% reduction in pain. Poor outcome with surgical intervention

Consults n Neurologic or orthopedic-spine surgery n Physical medicine and rehabilitation n Anesthesia Complications of treatment n Cauda equine syndrome n Arachnoiditis ossificans n Partial or complete paralysis and numbness of the lower extremities n Pain at rest n Constant burning pain in the lower extremities n Syringomyelia n Rare progression to paraplegia or death

Prognosis n n n n

Constant severe pain with significant disability Bladder dysfunction may develop later in the course of the disease. Increased risk of depression, suicide, and substance abuse Life span may be decreased up to 12 years.

Helpful Hints n

Poor response to analgesics

Suggested Readings Bourne IH. Lumbo-sacral adhesive arachnoiditis: a review. J R Soc Med. 1990;83(4):262–265. Burton CV. Lumbosacral arachnoiditis. Spine. 1978;3(1):24–30. Guyer DW, Wiltse LL, Eskay ML, Guyer BH. The longrange prognosis of arachnoiditis. Spine. 1989;14(12):1332–1341.


n

the meninges, and a soft tissue mass that replaces the subarachnoid space. MRI with gadolinium does not demonstrate signal changes with arachnoiditis, allowing differentiation from neoplasm. Myelography demonstrates loculations of contrast dye, loss of nerve root sleeves, and partial or total obstruction of dye flow.

13

Arteriovenous Malformation Description

Diagnosis

An arteriovenous malformation (AVM) is an abnormal collection of high-pressure arteries and veins without intervening capillaries that may enlarge or rupture.

Differential diagnosis n Intramedullary spinal tumor

Etiology/Types

n

n n

Glomerular types are the most common and are located superficially or within the spinal cord. Fistulous types are arteriovenous shunts most commonly found superficially on the spinal cord and are subcategorized into low- and high-shunt volume subtypes.

Epidemiology n n

Most common in patients over 30 years of age Male predominance

Pathogenesis n n

May be located throughout the spinal column Increased vascular pressure results in vessel enlargement resulting in spinal cord dysfunction.

History May be asymptomatic n Variable neurological deficits ranging from radiculopathy to myelopathy Exam Variable neurological deficits ranging from radiculopathy to myelopathy

n

Testing Spinal angiography is used for diagnosis and surgical planning. n MRI may not always be able to identify an AVM. n MRI can identify myelomalacia, edema, blood vessel thrombosis or thickening, and the presence of new bleeding n

Risk Factors n

Hereditary hemorrhagic telangiectasia

Clinical Features n n n n n n

Exercise claudication Occasionally associated with cutaneous angioma Bruit may be heard with auscultation over the spine. Venous congestion is associated with chronic and progressive myelopathy. Neurologic deficits may also be associated with spaceoccupying AVMs. Acute or chronic neurologic deficits may be associated with intramedullary or subarachnoid hemorrhage.


Progressive claudication, dysesthesias, and radicular pain Thrombosis of the vessels may result in symptom progression over several hours to weeks. Cervical AVM increases the risk of subarachnoid hemorrhage.

14

Sagittal cervical T2-weighted magnetic resonance image demonstrating an arteriovenous malformation within the spinal cord at the C4 level. (Adapted from Fast A, Goldsher D. Navigating the Adult Spine: Bridging Clinical Practice and Neuroradiology. New York: Demos Medical Publishing, 2007:130.)

Arteriovenous Malformation

n

CSF analysis may be normal or demonstrate red blood cells and increased protein. Electrodiagnostic testing may demonstrate multiple scattered bilateral radiculopathies of the thoracic, lumbar, and sacral nerve roots.

Pitfalls n Chronic myelopathy related to venous congestion may present with nonspecific neurologic changes making diagnosis difficult.

Red Flags n

Progressive neurologic deficits or myelopathy

Treatment

n n n

Surgical indications include progressive neurologic dysfunction and recurrent bleeding. Endovascular embolization Surgical resection with or without presurgical endovascular embolization

Consults n Neurologic or orthopedic-spine surgery Complications of treatment n Endovascular embolization and surgery decreases the risk of bleeding but increases the risk of further neurologic deterioration.

Prognosis n

Medical None

There is no data on the progression of asymptomatic AVMs.

n

Exercises n None Modalities None

n

Injection n None Surgical Asymptomatic AVMs should remain untreated.

n

Helpful Hints n

Progressive neurologic deficits or myelopathy should be evaluated and treated promptly.

Suggested Readings Bostroem A, Thron A, Hans FJ, Krings T. Spinal vascular malformations—typical and atypical findings. Zentralbl Neurochir. 2007;68(4):205–213. Zozulya YP, Slin’ko EI, Al-Qashqish II. Spinal arteriovenous malformations: new classification and surgical treatment. Neurosurg Focus. 2006;20(5):E7.


n

15

Atlantoaxial Instability Description Atlantoaxial instability (AAI) is characterized by increased motion at the atlas (C1) and axis (C2) interface, resulting from a bony or ligamentous abnormality.

Etiology/Types Three patterns of instability are flexion–extension, distraction, and rotation.

Epidemiology n n

n

Unknown prevalence in the general population Only 16% of atlantoaxial injuries result in neurologic deficits due to a large central spinal canal at this level. 15% of individuals with Down syndrome have laxity of the transverse ligament.

Pathogenesis n n n n

Stability is mainly provided by the transverse ligament and the two modified zygapophyseal (facet) joints. The transverse ligament and the odontoid process are the most common structures involved in instability. The alar ligament and tectorial membrane resist vertical displacement. Symptoms develop when the odontoid process or posterior arch of the atlas impinges on the spinal cord.

Risk Factors n n n n n n n n n

Cerebral palsy Down syndrome Dwarfism Grisel syndrome Klippel–Feil anomaly Larsen syndrome Neurofibromatosis Osteogenesis imperfecta Rheumatoid arthritis


History of head trauma Occipital pain in patients with rheumatoid arthritis Myelopathy

Natural History n

Asymptomatic patients with instability are not at higher risk of developing symptoms.

16

Diagnosis Differential diagnosis n Abnormal ossification or fracture of the odontoid n Tumors History Neck and/or suboccipital pain n Pain improved with supine positioning n Pain worsened with cervical range of motion n

Exam n Restricted neck range of motion n Tenderness overlying the C1–C2 articulation n Upper motor neuron findings with myelopathy Testing Open-mouth odontoid and lateral cervical spine X-rays n Transverse ligament rupture is noted if the combined spread of the lateral masses of C1 on C2 exceeds 6.9 mm. n Atlantodens interval (ADI) is the distance between the odontoid process and the posterior aspect of the anterior arch of the atlas measured on lateral X-rays. – Normally ≤3 mm in adults and ≤5 mm in children – Instability is present when there is an ADI difference of 3.5 mm or more on flexion/extension views. n Posterior atlantodental interval (PADI) measures the space available in the central canal and is the distance from the posterior border of the dens to the anterior border of the posterior tubercle. – Correlates with the degree of neurological deficits n CT and MRI can provide additional information on rotational AAI and spinal cord injury. n

Pitfalls Missed diagnosis

n

Red Flags n

Myelopathy

Treatment Medical n Preparticipation sports physicals are recommended for patients at risk. n The Special Olympics requires all children with Down syndrome to have neurologic and radiographic examinations to assess for AAI.

Atlantoaxial Instability

17

Exercises n None Modalities n None

A

Surgical n Posterior C1–C2 fusion is done with ligamentous injuries, as these ligaments have poor healing potential. n Surgery is most effective in patients with severe pain and mild signs of myelopathy. n Surgery is not recommended for patients without signs of myelopathy. n The indication for surgery in rheumatoid arthritis patients are atlantoaxial subluxation of >8 mm with cord compression, PADI 3.5 mm subaxial subluxation, or progressive neurological deficit. n Fusion is more extensive from the occiput to C2. Consults n Neurologic or orthopedic-spine surgery n Physical medicine and rehabilitation Complications of treatment n Spinal cord injury

Prognosis n

n n

Symptomatic patients are at increased risk of developing further neurologic deficits, yet paralysis and death are rare. Good functional prognosis following fusion surgery Early identification of a progressive myelopathy improves the functional prognosis.

Helpful Hints B

n

Lateral cervical flexion (A) and extension (B) plain radiographs demonstrating anterior subluxation of the odontoid process and the anterior arch of the atlas due to a fracture of the base of the odontoid process. (Courtesy of Keith Hentel, MD.)

Suggested Reading

No treatment required unless there are signs of spinal cord injury or compression.

Herman MJ, Pizzutillo PD. Cervical spine disorders in children. Orthop Clin North Am. 1999;30(3):457–466.


Injection n None

Aviation-Associated Back and Neck Pain Description Back and neck pain associated with aviation

Etiology/Types n

Thought to be related to vibration, prolonged static positioning, and poor posture

Epidemiology n

92% of young healthy aviators report back pain.

Diagnosis Differential diagnosis n Ankylosing spondylitis n Degenerative disc disease n Osteoarthritis n Osteoporosis n Rheumatoid arthritis History Progressive pain and discomfort during flight

n

Pathogenesis n

n

n

n

Sustained high Gz (acceleration due to gravity) maneuvers for 40 minutes have been found to decrease body height 4.9 mm and increase the risk of injury due to decreased intervertebral segment elasticity. Vibration is thought to lead to intervertebral disc microtrauma, which may predispose the disc to further injury. Pilot seats in commercial aircraft were designed to withstand excessive forces during accidents, but do not reportedly meet basic ergonomic design criteria. Most coach seats do not meet basic ergonomic design criteria.


Aircraft vibration during takeoff, landing, and turbulence Confined sitting position Helmet-mounted equipment Hoisting bags into overhead bins Physical deconditioning Prolonged static positioning Repeated exposure to accelerations exceeding 4.0 Gz Rushing through airports with heavy luggage

Clinical Features n

n

Typically neck and lower back range of motion will be decreased due to pain or restriction related to axial spine degenerative changes or tissue inflexibility. Paraspinal muscle spasm

Natural History n

Progressive pain and discomfort

18

Exam Normal motor, sensory, and reflex examinations n Tenderness in the cervical or lumbar paraspinal muscles n

Testing Imaging is done if the pain persists for several weeks or if weakness or numbness is found on examination. n Electrodiagnostic testing is used to assess for radiculopathy. n

Pitfalls Missing rheumatoid arthritis or ankylosing spondylitis

n

Red Flags n n

Severe weakness, numbness, or tingling Bowel or bladder dysfunction

Treatment Medical NSAIDs and relative rest for 24 hours after an acute injury or exacerbation n Prepositioning of the head and body prior to a high Gz maneuver n Postural and equipment modifications n Minimizing prolonged sitting during flight n Use of a pillow or rolled blanket for lumbar or thigh support n Luggage placed under the seat can be used as a footrest. n Business and first class commercial airline travel allows greater room to adjust seating comfort. n

Exercises Routine neck and lower back stretching and strengthening program

n


n

Injection Trigger point injections for symptoms of myofascial pain n Epidural steroid injections for radicular symptoms n

Surgical Discectomy n Fusion n

Consults Physical medicine and rehabilitation n Neurologic or orthopedic-spine surgery n General practitioner n

Complications of treatment n Progressive debilitating pain

Prognosis n

General aviation guidelines: – Pilots can return to flight duties once they are asymptomatic.

19

– Pilots are disqualified from flying if their low back symptoms are recurrent or chronic, have required hospitalization, and require regular medication beyond NSAIDs. n With nerve involvement or surgery, pilots will need to be asymptomatic for 6 weeks before they can be considered fit to return to flight status. n Fusion surgery can result in pilots being grounded for 6 months. n Pilots are permanently disqualified for multilevel discectomies. n Passengers may have significant difficulty flying after multilevel discectomies due to seat ergonomics.

Helpful Hints n

Early ergonomic modifications can safeguard against the development of a chronic pain condition.

Suggested Reading Mohler SR. Lower back pain is a common complaint, but precautionary practices help pilots cope. Hum Factors Aviat Med Flight Safety Foundation. 2000;47(3):1–6.


Aviation-Associated Back and Neck Pain

Baastrup’s Chapter Title Disease (Kissing Spines Disease) Description Baastrup’s disease is the development of a neoarthrosis between adjacent spinous processes.

Etiology/Types n

Caused by breakdown of the interspinous ligament

Epidemiology n n n n

More common with advancing age Young athletes Prevalence on autopsy ranges from 6.2% to 22.1% Most common at the L4 to L5 level

Diagnosis Differential diagnosis n Central spinal canal stenosis n Infection n Lumbar spondylosis n Muscle strain n Paracentral disc herniation n Spinous process fracture n Spondylolisthesis n Vertebral compression fracture History Localized interspinous or spinous process pain with or without a referral pattern

n

Pathogenesis n

n n

n

The supraspinous and intraspinous ligaments are sprained with extreme forward flexion, which may result in the development of a spur. Repetitive extension may disrupt the healing process. An interspinous bursae may develop due to supraspinous ligament laxity and intraspinous ligament breakdown. The interspinous ligament degenerates with aging resulting in the formation of a cavity, which can precede the development of pain.

Risk Factors n n n n n n n

Central spinal stenosis Degenerative disc disease Zygapophyseal (facet) joint osteoarthritis Gymnastics Hyperlordosis Paraspinal muscle atrophy Pars interarticularis defect

Exam Difficult to assess proximity of spinous processes on manual palpation due to their overlapping nature n Palpable tenderness of the supraspinous ligament with the patient in a side lying–fetal position n Pain with extension > flexion n

Testing Lateral plain radiographs may demonstrate sclerotic changes or flattening of adjacent spinous processes n MRI is useful to assess for interspinous edema or edema associated with early pars lesion; it can also rule out infection, tumor or a herniated disc. n Bone scanning with single-photon emission computed tomography (SPECT) can detect increased osteoblastic activity that is associated with reactive sclerosis. n

Pitfalls Pars interarticularis fracture n Spinous process fracture n Vertebral compression fracture n Lack of imaging findings n

Clinical Features n

Localized interspinous or spinous process pain with or without a referral pattern

Natural History n n

May be present for many years with progressive worsening over time The pain may be significant enough to limit activities of daily living.

20

Red Flags n

Infection

Treatment Medical n Bed rest in the semi-Fowler position (semiupright sitting position of 45 to 60 degrees with the knees either bent or straight)

Baastrup’s Disease


n

Injection Fluoroscopically guided diagnostic-interspinous injections have been used to confirm the diagnosis and for treatment. – Characteristic dye pattern is noted to be a cavity with a firm endpoint. – Injection may need to be repeated.

n

Surgical Cavity resection n Fusion n

Consults Physical medicine and rehabilitation

n

n

Neurologic or orthopedic-spine surgery

Complications of treatment n Complications related to surgery

Prognosis n

Unknown

Helpful Hints n

A clinical diagnosis, without findings on imaging may also be treated effectively with a corticosteroid/ anesthetic infiltration.

Suggested Readings Haig AJ, Harris A, Quint DJ. Baastrup’s disease correlating with diffuse lumbar paraspinal atrophy: a case report. Arch Phys Med Rehabil. 2001;82(2):250–252. Mitra R, Ghazi U, Kirpalani D, Cheng I. Interspinous ligament steroid injections for the management of Baastrup’s disease: a case report. Arch Phys Med Rehabil. 2007;88(10):1353–1356.


Exercises n Gentle strengthening and stretching n Flexion bias

21

Back Pain Associated with Dance Description

n

Back pain or injury that develops during dance training or performance

n n n

Etiology/Types n

Related to age and skill

n n n

Epidemiology n n n

Male predominance Spondylolysis is four times as common in dancers as compared to the general population. Increased incidence of spondylolysis with vigorous performance or rehearsals

Pathogenesis n n n

Repetitive microtrauma Injuries related to hyperlordosis occur with turning, jumping, or lifting. Male dancers develop upper back pain from strains due to lifting.

n

Discogenic back pain Infection Inflammatory spondyloarthropathies Neoplasm Sacroiliac joint pain Spondylolisthesis Spondylolysis Spondylosis

History Progressive pain during training or performance

n

Exam Pain from a pars interarticularis fracture is worsened with extension n Localized paraspinal muscle spasm n Hamstring tightness n Stepoff related to a spondylolisthesis n

Testing X-rays should include oblique views to assess for pars interarticularis fractures. n SPECT scan is indicated when there is a high suspicion of a pars interarticularis fracture with normal plain radiographs. n CT scan may also be used to assess zygapophyseal (facet) joint irregularity. n MRI is used to assess for stress fractures. n


Growth spurt resulting in decreased flexibility and musculotendinous tightening Hip joint abnormalities Hyperlordosis Improper footwear Leg-length discrepancies Musculotendinous imbalance Patellar misalignment Pes planus Training errors or significant changes in dance style, intensity, and frequency

Clinical Features n n n n

Hamstring tightness Pain from a pars interarticularis fracture is worsened with extension, especially in the arabesque position. Localized paraspinal muscle spasm Step off related to a spondylolisthesis

Natural History n

Progressive pain

Diagnosis Differential diagnosis Chondroplasia

n

22

Pitfalls Convincing dancers to decrease their dance intensity, duration, and frequency

n

Red Flags n n n

Undiagnosed fracture Radicular symptoms Unrelenting pain

Treatment Medical Assessment of a dancer’s technique and dance style to manage and prevent reinjury n Dancers with disabling pain or progressive neurologic decline should be managed as the general population. n Conservative treatment with grades 1 and 2 and asymptomatic grade 3 spondylolisthesis n

Back Pain Associated with Dance

Modalities n Muscle strains that occur during a performance may be treated with an ice massage or cold spray for symptomatic relief. n Heat, ultrasound, and transcutaneous electrical nerve stimulation have been used for symptomatic relief of pain and muscle spasms. Injection Trigger point injections for symptoms of myofascial pain n Epidural steroid injections for radicular symptoms

n

Surgical Discectomy n If pain from a pars fracture continues to be unresponsive to conservative treatments, fusion may be considered. n Surgical debridement of a pars interarticularis nonunion n Fusion is considered in symptomatic grade 3 and grade 4 spondylolistheses. n

Consults n Physical medicine and rehabilitation n Neurologic or orthopedic-spine surgery Complications of treatment n Dancers’ inability to return to their preinjury level of dance n Complications related to surgery

Prognosis n n n

Following discectomy, dancers may not be able to perform for up to one year. Return to professional dance will depend on the degree of recovery. Spondylolysis with grade 1 spondylolisthesis will remain stable and dancers can continue to dance safely although pain may be problematic.

Helpful Hints n n n

Prevention is important. Lordotic posturing should be monitored by dance instructors. Emphasis on core abdominal strengthening

Suggested Readings Hansen PA, Reed K. Common musculoskeletal problems in the performing artist. Phys Med Rehabil Clin N Am. 2006;17(4):789–801. Micheli LJ. Back injuries in dancers. Clin Sports Med. 1983;2(3):473–484.


Exercises Upper body and core abdominal muscle strengthening to decrease hyperlordosis and improve lifting technique n Antilordotic brace that is worn full time for 4 to 6 months but removed during training in dancers with a tight lordosis n Spondylolysis of less than 6 months duration is immobilized with an antilordotic brace. n Pilates n

23

Back Pain Associated with Golf Description

n

Back pain that develops during participation in golf

n

Etiology/Types

n

n

The golf swing generates a large rotational force that is controlled by the annulus fibrosis, zygapophyseal (facet) joints, musculotendinous, and fascial thoracolumbar stabilizers.

Osteoporotic vertebral body compression fractures Poor biomechanics resulting in greater torque and shear forces in amateurs Trunk muscle imbalance


Axial low back pain Pain with extension or rotation Pain during a golf swing

Epidemiology n n

Low back pain represents 26% to 52% of all golfrelated injuries. 30% of touring professional golfers play with low back pain

Pathogenesis

Natural History n

Diagnosis Differential diagnosis Central spinal stenosis n Degenerative disc disease n Fracture n Herniated nucleus pulposus n Neoplasm or metastasis n Radiculopathy

A golf swing requires lateral bending with axial compression and torsion, which is the most common cause of disc herniation. – The annulus fibrosis and zygapophyseal (facet) joints limit rotation. – Protective reflexive muscle stabilization can diminish with repetitive loading, resulting in creep and progressive laxity. – Laxity and decreased coordination of the thoracolumbar fascial stabilizers increases risk of injury. n In professional golfers, axial compression during a golf swing at the L3–L4 segment can be up to eight times body weight (7,584 ⫾ 2,422 N). – Disc prolapse in cadaveric studies can occur with only 5,448 N of axial compression. n Four basic components of the golf swing are the backswing, forward swing, acceleration with ball strike, and follow-through. n The modern golf swing, which generates greater force and distance, increases the hip–shoulder separation angle with a large shoulder turn and a restricted hip turn. n The classic golf swing reduces the hip–shoulder separation angle and the torque on the axial spine by raising the heel to increase the hip turn or shortening the backswing alone or in combination.

n

Risk Factors

n

n

n n n

Carrying a golf bag during play Constant practice sessions Decreased lead hip internal rotation

24

Progressive pain

History Axial low back pain with or without radiation

n

Exam Pain with extension or rotation n Pain during a golf swing n Paraspinal muscle spasm n Poor truncal strength n Decreased quadriceps or hamstring flexibility n Decreased hip range of motion n

Testing X-rays may be used to assess for degenerative changes or fracture, but can be nonspecific. n CT may be helpful in further delineating the bony anatomy or fracture. n MRI can be used to assess the intervertebral discs, nerve roots. and ligaments. n Electrodiagnostic testing can be used to assess for radiculopathy. n

Pitfalls Missed fracture

Red Flags n

Radiculopathy

Back Pain Associated with Golf

n

Fracture Bowel or bladder dysfunction

Treatment Medical Swing modifications n Gradual return with swinging short irons, practicing on the driving range, and trialing a 9-hole game prior to full 18 holes n Defer shots from deep rough, sand, or angled lies n During recovery, players should ride a golf cart or walk with a pull cart. n

Exercises n General strengthening and stretching with emphasis on core abdominal strengthening n Dynamic stabilization exercises targeting the transverse abdominus and multifidi muscles n Flexibility training in the older population Modalities n Heat, cold, ultrasound, and transcutaneous electrical nerve stimulation have been used for symptomatic relief of pain and muscle spasms. Injection n Trigger point injections for symptoms of myofascial pain n Epidural steroid injection for radicular symptoms

n

Medial branch blocks/radiofrequency neurotomy for zygapophyseal (facet) joint–mediated pain

Surgical Fusion

n

Consults n Physical medicine and rehabilitation n Neurologic or orthopedic-spine surgery Complications of treatment n Adjacent level disease following lumbar fusion may be accelerated with golfing activities.

Prognosis n n

Following a laminectomy, a player can begin swinging a club at 6 to 12 weeks. Lumbar fusion patients are restricted from swinging a club for at least 6 to 12 months postoperatively.

Helpful Hints n

Golf is not a benign sport.

Suggested Readings Gluck GS, Bendo JA, Spivak JM. The lumbar spine and low back pain in golf: a literature review of swing biomechanics and injury prevention. Spine J. 2007. Parziale JR, Mallon WJ. Golf injuries and rehabilitation. Phys Med Rehabil Clin N Am. 2006;17(3):589–607.


n

25

Back Pain Associated with Heavy Loads Description

Natural History

Back pain related to lifting or maneuvering heavy loads

n

Etiology/Types

Diagnosis

n

Repetitive lifting changes muscle recruitment patterns resulting in poor spinal loading patterns, which increases the risk of injury.

Epidemiology n

33% of all work-related back pain events are caused by lifting or bending.

Pathogenesis Squat lift, with the knees bent and back straight, is considered safer than the stoop lift, with the knees straight and back bent. – Minimal research supports the squat lift over the stoop lift. n Most workers prefer the stoop lift as the squat lift results in more rapid fatigue. – Greater extensor muscle activity results in greater fatigue due to repetitive or sustained loading. n Increased muscle activity and/or an increased intraabdominal pressure increases spinal stability. n Momentary loss of spinal stability can lead to unexpected displacement in the spine, resulting in injury. n

Risk Factors n n n n n n n n n n

Awkward posture Cognitive, emotional, and psychosocial factors Fatigue High-stress work environment Increased trunk velocity Inadequate lifting strength of an individual compared to the occupational lifting demands Lifting with twisting or lateral bending Low job satisfaction Poor social support Very heavy loads


Patients primarily complain of axial low back pain with or without radiation into the lower extremities. Hypertrophy of the paraspinal extensor group indicates increased load on these muscles. Associated with pain complaints in other regions of the body

26

Progressive axial low back pain

Differential diagnosis n Central spinal stenosis n Degenerative disc disease n Fracture n Herniated nucleus pulposus n Neoplasm or metastasis n Radiculopathy History Axial low back pain n Muscle spasm n

Exam n Decreased lumbar flexion and extension due to pain n Body asymmetry n Tenderness to palpation of the paraspinal muscles n Paraspinal hypertrophy Testing n Not generally required in nonspecific low back pain, although important if pain has not improved within 4 to 6 weeks. n Usefulness of MRI in nonspecific low back pain is questionable, as degenerative findings are common in asymptomatic subjects. n Electrodiagnostic study to assess for a radiculopathy Pitfalls Increasing time off from work

n

Red Flags n n n

Bowel or bladder dysfunction Fracture Radiculopathy

Treatment Medical Ergonomic assessment of the work-station or workplace n Short-term NSAIDs n

Exercises Training programs can reduce the incidence of back pain in the workplace.

n

Back Pain Associated with Heavy Loads

n n

Work hardening may be indicated to strengthen weak muscles. Proper lifting instruction Instructions in safe lifting techniques should include a plan for the lift, keeping the load close to the body, avoiding twisting, and bending at the knees.


n

Injection n Trigger point injections for symptoms of myofascial pain n Epidural injections for symptoms related to radiculitis or stenosis Surgical n None Consults Physical medicine and rehabilitation

n

Complications of treatment n Progressive work disability

Prognosis n

n

The prognosis can be good if the causes are related to ergonomic factors or lack of body mechanics or body awareness with lifting. Poor prognosis if psychosocial or social factors play a significant role and are not addressed.

Helpful Hints n

Address workplace ergonomics and possible additional psychosocial stressors that may be contributing factors.

Suggested Readings Arjmand N, Shirazi-Adl A. Biomechanics of changes in lumbar posture in static lifting. Spine. 2005;30(23):2637–2648. Schenk P, et al. Symptomatology of recurrent low back pain in nursing and administrative professions. Eur Spine J. 2007.


n

27

Back Pain Associated with Occupation Description

n

Back pain associated with tasks in the workplace

n n

Etiology/Types n

Generally unknown

Epidemiology n n

Most common cause of disability in adults aged 45 years or younger Patients covered by worker’s compensation plans tend to have greater health care utilization and a longer duration of recovery compared to other forms of insurance.

n n

Degenerative disc disease Fracture Herniated nucleus pulposus Neoplasm or metastasis Radiculopathy

History n Difficult to ascertain work relatedness, the recurrence of a previous injury, or the onset of a systemic illness n Review previous visits to the emergency room or hospital stays Exam Decreased lumbar flexion and extension due to pain n Paraspinal hypertrophy n Tenderness to palpation of the paraspinal muscles n Body asymmetry n Waddell’s nonorganic signs (distraction. overreaction, regionalization, simulation, and tenderness) n

Pathogenesis n n n

Low back strain Radiculopathy Zygapophyseal (facet) joint pain

Risk Factors n n n n n n n n n n n

Bending Cognitive, emotional, and psychosocial factors High-stress work environment Inadequate lifting strength of an individual compared to the occupational lifting demands Low job satisfaction Manual lifting Poor social support Smoking Twisting Very heavy loads Whole body vibration

Testing Not generally required in nonspecific low back pain, although important if pain has not improved within 4 to 6 weeks. n The usefulness of MRI in nonspecific low back pain is questionable as degenerative findings are common in asymptomatic subjects. n

Pitfalls An inadequate history and physical examination can lead to poor treatment outcomes and recurrent injury. n Pending or ongoing litigation acts as an incentive to minimize recovery, continue diagnostic testing, and overvalue surgical intervention. n

Clinical Features n n

Patients primarily complain of axial low back pain with or without radiation into the lower extremities. Hypertrophy of the paraspinal extensor group indicates increased load on these muscles.

Red Flags n n n n

Natural History n

n

Associated febrile illness Cauda equina syndrome Fracture Numbness or tingling Weakness


Treatment Diagnosis Differential diagnosis Central spinal stenosis 28

n

Medical Advice to remain active n NSAIDs n

Back Pain Associated with Occupation

n n n

Muscle relaxants Analgesics Workstation assessment Acupuncture has been described as being helpful.

Exercises Initial passive treatments should progress to active strengthening and stretching with a major emphasis on developing a home exercise program.

n

Modalities n Heat, cold, ultrasound, and transcutaneous electrical nerve stimulation have been used for symptomatic relief of pain and muscle spasms. Injection n Trigger point injections for symptoms of myofascial pain n Epidural steroid injection for radicular symptoms

n

Complications of treatment Inability to return to preinjury occupation

n

Prognosis n n n n

Consults n Referral to a multidisciplinary rehabilitation program, if there is difficulty returning to work after 4 to 12 weeks n Physical medicine and rehabilitation

85% of the total medical costs result from only 10% of patients with back pain of >3 months duration. Most patients with low back pain will recover within 4 to 6 weeks. 85% of patients will have symptom recurrence over their lifetime. A worker with a poor evaluation from an immediate supervisor within 6 months is most predictive of poor return to work status.

Helpful Hints n

Surgical n None acutely unless there is a surgical lesion

Neurologic or orthopedic-spine surgery for clear surgical pathology

Complete pain relief should not be a limiting factor for return to work.

Suggested Readings Bigos SJ, Battie MC, Spengler DM, et al. A longitudinal, prospective study of industrial back injury reporting. Clin Orthop Relat Res. 1992;(279):21–34. Nadler S, Stitik T. Occupational low back pain: history and physical examination. Occup Med. 1998;13(1):61–81.


n

29

Back Pain Associated with Pregnancy Description Back pain that is related to the unique changes associated with pregnancy

Etiology/Types n n n n

Ligamentous laxity due to the hormone relaxin Sacroiliac joint dysfunction Lumbar disc herniation Degenerative spondylolisthesis

Epidemiology n n n

Estimates vary widely Incidence rate of low back pain in pregnancy can approach 50%. 30% to 45% of women in the postpartum period report low back pain.

Pathogenesis n

n

n

n n

Gravid uterus causes compensatory lumbar lordosis resulting in mechanical strain on the lower back and increased pelvic rotation. Relaxin is secreted by the corpus luteum resulting in ligamentous laxity and relaxation of the pelvic and sacroiliac joints. Prolonged supine positioning leads to obstruction of the vena cava, allowing venous congestion and hypoxemia, resulting in the development of lumbar pain. Lumbar disc herniation is the proximal source of pain in 1 in 10,000 cases of pregnancy-associated back pain. Pregnancy may also accelerate the development of a degenerative spondylolisthesis.

Risk Factors n n n

Increasing maternal age Number of previous births Previous history of back pain with pregnancy


Most common during the fifth to seventh month of pregnancy 46% describe radiation in the lower extremities Pain worsened with standing, sitting, forward flexion, lifting, and walking.

Natural History n

Increasing pain with pregnancy that generally improves postpartum

30

Diagnosis Differential diagnosis n Discogenic pain n Hip joint pathology n Lumbar disc herniation n Mechanical strain n Pelvic ligamentous laxity n Sacroiliac joint pain n Spondylolisthesis History Lumbar of pelvic/sacroiliac pain with possible posterior thigh or inguinal radiation n Improved with sitting, recumbency, or the use of a supportive pillow n

Exam Positive sacroiliac compression test n Pain with bilateral compression over the iliac crests n Positive Patrick’s test n Paraspinal muscle spasm n Step-off deformity with spondylolisthesis n

Testing Noncontrast MRI may be performed with no recognized harm to the developing fetus; long-term consequences are unknown.

n

Pitfalls Diagnosis is primarily based on clinical examination due to limitations of additional testing.

n

Red Flags n n n n

Bowel and bladder dysfunction Cauda equina syndrome Infection Weakness, numbness, or tingling

Treatment Medical Activity and postural modifications n Abdominal binders that help support the uterus n Sacroiliac joint belt to stabilize the sacroiliac joint n Oral pain medication should be coordinated with the obstetrician. n Antiprostaglandins are contraindicated during pregnancy as they may cause a premature closure of the ductus arteriosus. n

Back Pain Associated with Pregnancy

Acetaminophen is often the pain reliever of choice.

Exercises n Exercise program focused on muscle imbalance and alignment of the pelvic girdle n Pelvic tilts n Aquatic exercise n Sacroiliac joint mobilization Modalities Heat, transcutaneous electrical nerve stimulation, ultrasound are contraindicated.

n

Injection Could consider an intralaminar epidural steroid without fluoroscopic guidance by an experienced practitioner

n

Surgical n Discectomy n Laminectomy Consults Physical medicine and rehabilitation n Neurologic or orthopedic-spine surgery for cauda equina or progressive neurologic deterioration n

Complications of treatment n Postpartum weakness, numbness, or tingling

Prognosis n n

Very good prognosis for improvement within the first weeks after delivery Biopsychosocial factors may play a role in determining prognosis.

Helpful Hints n

Regular exercise before pregnancy can reduce the risk of back pain.

Suggested Readings Bastiaanssen JM, de Bie RA, Bastiaenen CH, Essed GG, van den Brandt PA. A historical perspective on pregnancyrelated low back and/or pelvic girdle pain. Eur J Obstet Gynecol Reprod Biol. 2005;120(1):3–14. Borg-Stein J, Dugan S, Gruber J. Musculoskeletal aspects of pregnancy. Am J Phys Med Rehabil. 2005;84:180–192. Fast A, Shapiro D, Ducommun EJ, Friedmann LW, Bouklas T, Floman Y. Low-back pain in pregnancy. Spine. 1987;12(4):368–371.


n

31

Back Pain Associated with Sitting Description

Clinical Features

Back pain associated with prolonged sitting or sitting on improper surfaces

n

Etiology/Types

n

Axial low back pain that is worsened with sitting

Natural History n


Multifactorial

Diagnosis Epidemiology n

75% of workers in industrialized countries are involved in sedentary jobs that require prolonged sitting.

Pathogenesis n

n

n

n n

n

n n

No evidence that sitting up “straight” or having “good posture” with a lumbar support is beneficial, although it is generally advised. Lower incidence of lumbar disc degeneration in populations that sit or squat with a compensatory flattening of the lumbar lordosis. Inactivity related with prolonged sitting is thought to decrease fluid flow across the endplates resulting in the accumulation of intradiscal metabolic byproducts causing accelerated disc degeneration. Prolonged sitting leads to static loading of soft tissues. Loss of the protective stabilizing reflexes of the multifidi with stretching of the viscoelastic structures Reclined seating allows some body weight to be transferred to the back rest and reinforces the lumbar lordosis. Intradiscal pressures are 35% higher, if sitting with no lumbar support as compared with standing. The work task has a great influence on muscle activity and lumbar disc pressure.


Awkward posture Decreased physical conditioning Driving may be a risk factor Tall stature Obesity Pregnancy Prolonged sitting Psychological and physiological stress Smoking Whole body vibration

32

Differential diagnosis Central spinal stenosis n Degenerative disc disease n Fracture n Herniated nucleus pulposus n Neoplasm or metastasis n

History n Low back pain with sitting n Low back pain that is better in the morning, worsens as the day progresses or with prolonged sitting Exam Rounded shoulders and a head forward posture with sitting n Significant hamstring tightness is common n Ely’s test often uncovers quadriceps tightness n Pain-limited lumbar flexion and extension n Poor core stabilization demonstrated by uncoordinated hip extension while prone; normally there should be activity first at the erector spinae, followed by the gluteus medius, then the muscles of the hamstring complex. n

Testing Not generally required in nonspecific low back pain although important if pain has not improved within 4 to 6 weeks. n The usefulness of MRI in nonspecific low back pain is questionable as degenerative findings are common in asymptomatic subjects n

Pitfalls Not addressing the seated work environment during the initial clinical visit

n

Red Flags n n n n

Bowel or bladder dysfunction Fracture Infection Radiculopathy

Back Pain Associated with Sitting

Medical n Sitting posture factors include the design of the chair, routine sitting habits, seat height and inclination, the position of the back rest, other supports as well as the work task. n Chair design should include lumbar support and allow the occupant to easily adjust the seating surface. n Use of arm rests and lumbar support reduce the pressure on the lumbar spine. n Whole body vibration can be reduced using vibration isolation seats. n Poor driver visibility and poor positioning of the controls requiring increased twisting and stretching should be addressed. n Acupuncture has been described to be helpful. Exercises n General strengthening and stretching with emphasis on core abdominal strengthening to maintain good strength and endurance as well as coordination Modalities n Heat, cold, ultrasound, and transcutaneous electrical nerve stimulation have been used for symptomatic relief of pain and muscle spasms.

Injection n Trigger point injections for symptoms of myofascial pain Surgical None

n

Consults n Physical medicine and rehabilitation n Ergonomist Complications of treatment n Continued progressive axial low back pain

Prognosis n

The prognosis is good if the underlying factors are identified.

Helpful Hints n

Prevention is important.

Suggested Readings Lis AM, Black KM, Korn H, Nordin M. Association between sitting and occupational LBP. Eur Spine J. 2007;16(2):283–298. Pope MH, Goh KL, Magnusson ML. Spine ergonomics. Annu Rev Biomed Eng. 2002;4:49–68.


Treatment

33

Back Pain Associated with Soccer Description

n

Back pain that occurs with participation in the sport of soccer

n n n

Etiology/Types n n n n n n

Cyclic loading with repetitive activities Muscle sprain or strains are the most common. Spondylosis Spondylolisthesis Spondylolysis Sacroiliac joint dysfunction

Epidemiology n n

Soccer is the fastest growing sport in the United States and the most popular sport in the world. Low back pain is the third most common soccer injury after knee and ankle injuries, respectively.

Pathogenesis n n n

Players often note that their pain begins after a highvelocity kick. Sprains result from eccentric overload of the paraspinal muscles. Hip extension strength is often weaker following an episode of low back pain, increasing the risk of further injury.

Risk Factors n n n n n

Decreased abdominal core strengthening Hamstring strength imbalance (hip extensor strength) Leg-length discrepancy Prior back strain Sacroiliac joint rotation


Muscle strain or sprain results in localized muscle pain or spasm. Spondylosis, spondylolisthesis, or spondylolysis can refer pain to the buttocks or posterior thigh with rare radiation below the knee.

Natural History n

Axial low back pain may resolve or progressively worsen

Diagnosis Differential diagnosis n Central spinal stenosis

34

n n

Degenerative disc disease Fracture Herniated nucleus pulposus Lumbar paraspinal sprain or strain Neoplasm or metastasis Radiculopathy

History Pain worsened with running or kicking

n

Exam Hip extensor strength imbalance n Stepoff deformity associated with spondylolisthesis n

Testing Anteroposterior (AP) and lateral X-rays allow for assessment of vertebral body listhesis or dislocation. n Oblique X-rays can assess osteoarthritic changes in the zygapophyseal (facet) joints or a defect of the pars interarticularis. n MRI is useful to look at soft tissue elements of the spine including the ligaments and intervertebral discs. n SPECT is used to detect a clinically suspected spondylolysis that has not been found on X-rays. n Electrodiagnostic studies are useful in assessing for a potential radiculopathy. n

Pitfalls Diagnostic difficulty

n

Red Flags n n n

Radiculopathy Fracture Bowel or bladder dysfunction

Treatment Medical Heel lift for a leg-length discrepancy n Sacroiliac joint mobilization n Thoracolumbar bracing, commonly the use of a Boston brace, may be used for pain control in spondylolysis/spondylolisthesis. n The bracing would have to be worn for 23 hours of the day. n Acupuncture has been described to be helpful with associated muscle spasm. n

Exercises Core abdominal stabilization exercises to allow the player to stabilize the lumbopelvic region

n

Back Pain Associated with Soccer

n

Hamstring strengthening with a focus on developing symmetric strength Training focused on developing endurance and power

Modalities n Heat, cold, ultrasound, and transcutaneous electrical nerve stimulation have been used for symptomatic relief of pain and muscle spasms. Injection Trigger point injections for symptoms of myofascial pain n Epidural steroid injection for radicular symptoms n

Surgical n Laminectomy for radiculopathy n Repair of the pars interarticularis for spondylolysis Consults n Physical medicine and rehabilitation n Neurologic or orthopedic-spine surgery Complications of treatment Progression of the a stress fracture to a full pars interarticularis fracture

n

Prognosis n n n

Spondylolysis requires the discontinuation of participation for 3 months. Discontinuation of the sport can be more effective than bracing. 78% to 92% of young participants with spondylolysis are able to return to full activities, but only 18% to 37% demonstrated evidence of bony healing.

Helpful Hints n n n

The most common injury is a muscle strain or sprain. Spondylolysis is common in the soccer player due to the repetitive lumbar extension. Important to assess hamstring flexibility and strength

Suggested Readings El Rassi G, Takemitsu M, Woratanarat P, Shah SA. Lumbar spondylolysis in pediatric and adolescent soccer players. Am J Sports Med. 2005;33(11):1688–1693. Manning MR, Levy RS. Soccer. Phys Med Rehabil Clin N Am. 2006;17(3):677–695.


n

35

Back Pain Associated with Tennis Description

Risk Factors

Back pain that occurs with participation in the sport of tennis

n n n

Etiology/Types n

Continuous microtrauma from repetitive loading and rotation with hyperextension

n n

Hamstring injury or inflexibility Lumbar inflexibility Muscle fatigue Repetitive muscle contraction Shoulder injury

Clinical Features Epidemiology n n

38% of 148 professional tennis players missed a tournament due to back pain. Unknown if tennis players have a higher risk of back pain compared to the general population.


n n

n

n n n

n

The serve causes the greatest stress on the lumbar spine. Traditional forehand groundstroke results in 90 degrees of axial spine rotation. The open-stanced forearm swing involves more rotational acceleration as there is less trunk rotation. The one-handed backhand requires less trunk rotation as the hitting shoulder is already facing the net. Grass courts and increased ball speed increase axial hyperextension. Zygapophyseal (facet) joint arthropathy on imaging was found in 70% of asymptomatic elite young tennis players, mean age 17 years, compared to 8% to 21% found in an asymptomatic general population with a mean age of 35 to 43 years. Pars interarticularis stress injuries are the second most common type of injuries in tennis due to excessive hyperextension during the serve. Disc degeneration in young elite tennis players is similar to nonelite athletes Spondylolisthesis occurs in 6% of asymptomatic elite young players. Asymmetrical loading occurs due to the forces generated by the dominant hitting shoulder on the nondominant side of the trunk, resulting in increased strength in the dominant forearm and increased external rotation with decreased internal rotation of the dominant shoulder. Smooth rotation with flexion–extension occurs through alternating and coordinated concentric– eccentric muscle action.

36

n n

Lumbar strain results from a change in the intensity, duration, or technique during play. Sudden onset of symptoms; sometimes the onset of pain may follow a change in the normal routine after only a short period of time.

Natural History n

Axial low back pain may resolve or progressively worsen.

Diagnosis Differential diagnosis Degenerative disc disease n Herniated nucleus pulposus n Pars interarticularis stress reaction n Radiculopathy n Spondylolisthesis n Spondylolysis n Spondylosis n

History Lumbar strain or spondylosis may present as unilateral or bilateral lower back pain with or without a referral pattern.

n

Exam Lumbar shift away from the painful side n Concave spinal curvature toward the side of pain n Symmetry of the posterior superior iliac spines should be documented. n Lumbar flexion may be pain limited n Pain free lumbar extension if the zygapophyseal (facet) joints are not affected n Shoulder range of motion should be assessed. n

Testing Imaging is considered in patients with chronic back pain or signs of nerve root involvement. n Oblique X-rays are used to assess the zygapophyseal (facet) joints. n

Back Pain Associated with Tennis

n

MRI is useful in assessing acute or chronic pars interarticularis injuries and to determine healing potential. Electrodiagnostic studies should be completed on players with neurologic deficits.

Pitfalls Diagnostic difficulty

n

Red Flags n n n


Treatment Medical Acute pars interarticularis stress responses can be limited with refraining from play. n Injuries of the pars interarticularis respond better to treatment if recognized early. n NSAIDs n Analgesics n Bracing for pars interarticularis fractures n Acupuncture has been described as helpful for associated muscle spasm. n

Exercises n General strengthening and stretching with emphasis on core abdominal strengthening n Dynamic stabilization exercises with emphasis on strengthening of the muscles in the shoulder and lower extremities as well as the core abdominal muscles Modalities Heat, cold, ultrasound, and transcutaneous electrical nerve stimulation have been

n

used for symptomatic relief of pain and muscle spasms. Injection n Trigger point injections n Epidural steroid injection for radicular symptoms Surgical n Laminectomy for radiculopathy n Repair of the pars interarticularis for spondylolysis Consults n Physical medicine and rehabilitation n Neurologic or orthopedic-spine surgery, if there has been no improvement with conservative treatment. Complications of treatment Progression of a pars interarticularis stress response to a full fracture

n

Prognosis n

A player may return to play within several days after an uncomplicated acute lumbar strain.

Helpful Hints n n

Acute pars interarticularis stress responses can be limited with refraining from play. Emphasis on dynamic stabilization exercises for strengthening the shoulder stabilizer muscles, lower extremities, and the core abdominal muscles that connect these two areas.

Suggested Reading Perkins RH, Davis D. Musculoskeletal injuries in tennis. Phys Med Rehabil Clin N Am. 2006;17(3):609–631.


n

37

Back Pain in Mature Athletes Description

n

Back pain that occurs in mature populations that engage in sports

n n n

Etiology/Types n

Variable

n n n


Most common injury is muscular strain or sprain Prevalence of back pain in former elite athletes is 29% compared to 44% for nonathletes. 1% to 9% prevalence in runners 37% prevalence in soccer players 32% to 38% prevalence in tennis players 27% prevalence in American football players within an 8-year period

n n n n

Degenerative disc disease Infection Pancreatitis Pars interarticularis stress reaction Posterior penetrating stomach ulcers Radiculopathy Renal disease Spinal stenosis Spondylolisthesis Spondylolysis Spondylosis

History In general, the pain may present as unilateral or bilateral lower back pain with or without a referral pattern.

n

Exam Antalgic gait n A step-off at adjacent spinous processes may suggest a compression fracture. n Hip internal and external rotation to screen for underlying intra-articular hip pathology n Beyond age 30 the straight leg raise is found to be less reliable. n Bilateral loss of the ankle reflexes is often a result of advanced age. n A sacral stress fracture may be worsened with Patrick’s test and pain with hopping on the involved side. n Abdomen should be palpated to rule out the possibility of an abdominal aortic aneurysm. n Assess for peripheral vascular disease n

Pathogenesis n n

Sports that require compressive loads with flexion and rotation increase the risk of disc degeneration. Calcification and osteophytes develop as the body attempts to autostabilize the segment.

Risk Factors n n n n n n

Changes in an athlete’s training schedule Decreased hamstring flexibility Impaired lower extremity biomechanics Wrestling, weight lifting, and gymnastics Muscle imbalance There is no specific association between sports and spinal stenosis.


Pain may develop due to a change in the intensity, duration, or technique during play. Sudden onset of symptoms; sometimes the onset of pain may follow a change in the normal routine after only a short period of time.

Natural History n

Axial low back pain may resolve or progressively worsen.

Diagnosis Differential diagnosis Colorectal and gynecological malignancies

n

38

Testing Lab tests for sacroiliac joint pain may include laboratory studies such as a complete blood count, C-reactive protein, and erythrocyte sedimentation rate. n X-rays of the lumbosacral spine should be considered in cases of direct trauma, midline pain, or lower back deformity. n A study of MRIs of asymptomatic athletes aged 41 to 69 years, who were active triathletes or handball players, demonstrated similar degenerative changes compared to the general population. n Former elite soccer players and weight-lifting athletes demonstrate increased degenerative changes compared with the general population. n Electrodiagnostic studies can assess for possible nerve root lesions or peripheral neuropathy. n

Back Pain in Mature Athletes

Red Flags n n n


Treatment Medical n Short-term NSAIDs n Muscle relaxants n Analgesics n Bracing for spondylolysis n Acupuncture has been described as helpful. Exercises General strengthening and stretching with emphasis on core abdominal strengthening n Dynamic stabilization exercises targeting the transverse abdominus and multifidi muscles n Sports specific exercises and plyometrics n


n

Injection n Trigger point injections for symptoms of myofascial pain n Medial branch blocks/radiofrequency neurotomy for zygapophyseal (facet) joint–mediated pain n Epidural steroid injection for radicular symptoms

Surgical n Dependent on injury or chronicity Consults n Physical medicine and rehabilitation n Neurological or orthopedic-spine surgery Complications of treatment n Variable

Prognosis In most athletes the pain is self-limiting. Compression fractures are generally stable if only the anterior column is disrupted with >20 degrees of kyphosis. – Athlete may return to noncontact sport when they are painfree and may fully return once the fracture has healed in about 6 to 8 weeks. n Athletes with mild to moderate spinal stenosis may safely return to activity with a program of core strengthening exercises. n A surgical approach at one level may also allow full return to sport. n Multilevel surgical treatment may limit or prevent return to sports activities due to adjacent level degeneration. n n

Helpful Hints n

Athletes should be instructed to listen to their bodies.

Suggested Reading Hackley DR, Wiesel SW. The lumbar spine in the aging athlete. Clin Sports Med. 1993;12(3):465–468.


Pitfalls Only 15% of mature athletes with back pain have a precise pathoanatomical diagnosis.

n

39

Back Pain in the Older Population Description

Natural History

Back pain that occurs in the older population

n

Etiology/Types

Diagnosis

n

Variable

Epidemiology n

n n n

n

Back pain correlates with functional deficits, future disability, and the perception of ease in performing activities of daily living. One-year prevalence of back pain is about 31.5% in persons aged 65 years and older. 18% to 34% of individuals aged 70 years or older report functional limitations related to back pain. Reported back pain is higher among women than among men, possibly related to an increased risk of osteoporosis and vertebral compression fractures and complaining being more socially acceptable than in men. Prevalence of back pain decreases at 85 years of age in women and 90 years in men; possibly related to memory deficits, decreased physical activity, and the overshadowing of other medical problems.

Pathogenesis n

Progressive degenerative cascade as described by Kirkaldy–Willis


Deconditioning related to acute or chronic illness Decreased lower extremity strength Genetics only mildly influences the development of back pain in older twins. Increased depressive symptoms Osteoporosis Smoking

Clinical Features n n n n n n n n

Axial lower back pain Decreased lumbar flexion and extension Loss of lumbar lordosis 95.5% demonstrate myofascial pain. 83.6% demonstrate sacroiliac joint pain. 48% demonstrate hip pain. 19% demonstrate tender points that correlate with fibromyalgia. 26% demonstrate lumbar spinal stenosis.

40


Differential diagnosis n Central spinal stenosis n Degenerative disc disease n Fracture n Herniated nucleus pulposus n Myofascial pain n Neoplasm or metastasis n Radiculopathy n Spinal stenosis n Spondylolisthesis n Trochanteric bursitis n Zygapophyseal (facet) joint–mediated pain History Axial lower back pain n Improvement with recumbency n Worsened with activity n

Exam Decreased lumbar flexion and extension n Thoracic kyphosis n Loss of lumbar lordosis n Paraspinal muscle spasm may be associated with an underlying vertebral body compression fracture. n Patient’s ability to roll over gives a good indication of their baseline functional mobility. n Often tenderness is noted in the gluteus medius and trochanteric region. n

Testing X-rays are useful for the assessment of vertebral body compression fracture. n MRI is useful to assess for underlying soft tissue abnormalities and neoplasms. n With increasing age, abnormal findings increase on imaging studies. n

Pitfalls Difficulty correlating clinical diagnosis with imaging findings

n

Red Flags n n

Radiculopathy Fracture

Back Pain in the Older Population

n n

Bowel or bladder dysfunction Infection Neoplasm

n n n

Treatment Medical Females are more likely to use pain medication n Short-term NSAIDs n Muscle relaxants n Analgesics, although caution should be taken with cognitive changes. n Caution with pain medications as they may interact with other prescription medications n Acupuncture has been described to be helpful. n Long-term pain management may be required to maintain functional mobility. n

Exercises Focus on treating leg-length discrepancy, poor posture, or poor body mechanics n Moderate physical activity n “McKenzie” style mechanical evaluation to determine a direction of preference n With osteoporosis, there may be restrictions on the degree of overpressure and manual techniques that can be applied. n


Zygapophyseal (facet) joint injections Medial branch blocks/radiofrequency neurotomy Epidural steroid injection for radicular symptoms

Surgical n Decompressive surgery may be indicated for spinal stenosis. n Percutaneous vertebral augmentation may be indicated for unrelenting pain from a vertebral body compression fracture. Consults Physical medicine and rehabilitation n Neurological or orthopedic-spine surgery n Pain management n Geriatrics n

Complications of treatment n Variable

Prognosis n

Prognosis is based on the underlying pathology.

Helpful Hints n

Older adults should participate in regular moderate aerobic physical activity, strength, and flexibility training.

n

Injection Trigger point injections for symptoms of myofascial pain

n

Suggested Reading Hartvigsen J, Christensen K. Active lifestyle protects against incident low back pain in seniors: a population-based 2-year prospective study of 1387 Danish twins aged 70–100 years. Spine. 2007;32(1):76–81.


n

41

Back Pain in Young Athletes Description

n

Back pain that occurs in younger athletes


Spondylolytic lesions Lordotic back pain Muscle strain or sprain

Epidemiology n n

n n

In athletes under 12 years of age, a pathologic spondylolytic lesion is noted in up to 50% of cases. Prevalence of back pain in the adolescent athlete is 46% compared to the age-matched nonathlete, which is 18%. 47% of adolescent low back pain is related to spondylolysis compared to 5% of the adult population. Lordotic back pain is the second most common cause of back pain in the adolescent athlete.

Pathogenesis Spondylolysis is most commonly unilateral affecting the L5–S1 segment followed by the L4–L5 segment. n Low-level repetitive stresses or forceful extension with rotation can fracture the pars interarticularis, irrespective of an inciting event. n Spondylolisthesis occurs due to a pars interarticularis defect or elongation and can progress during the preadolescent growth spurt. n Lordotic back pain occurs as the growth spurt continues elongating the axial spine, resulting in tightening the thoracolumbar fascia. – Tissue tightness causes a traction apophysitis at the iliac crest or spinous process and may also impinge the adjacent spinous processes resulting in a pseudoarthrosis.

n

Risk Factors n

Spondylotic lesions—family history, Alaska natives, repetitive hyperextension in sports such as dance, gymnastics, football, and figure skating


Low back pain of intermittent episodes and of increased severity The pain of a spinous process fracture is usually worse than a muscle spasm.

42

Lordotic back pain and muscle strain or sprain is a diagnosis of exclusion.

Natural History n

Variable

Diagnosis Differential diagnosis Abdominal or genitourinary pathology n Ankylosing spondylitis n Apophyseal ring fractures n Disciitis n Herniated nucleus pulposus n Juvenile rheumatoid arthritis n Lymphoma n Neuroblastoma n Osteosarcoma n Psychogenic low back pain n Scheuermann’s kyphosis n Spinous process fractures n Spondylolysis or spondylolisthesis n Vertebral osteomyelitis n

History Variable

n

Exam n Gait assessment should include heel and toe walking – Trendelenburg gait n Assess for scoliosis, kyphosis, or pelvic obliquity n Hamstring tightness may manifest with a stiff-legged gait with a short stride n Step-off deformity if the spondylolisthesis is severe. n Pars interarticularis defect will cause pain with an ipsilateral one-legged hyperextension test. n Hyperlordosis of the lumbar spine may be present. Testing Oblique X-rays may demonstrate a pars interarticularis fracture. n MRI is considered for herniated nucleus pulposes, disciitis, vertebral osteomyelitis and bone marrow edema which is an early sign of a pars interarticularis stress reaction. n SPECT is the most sensitive test to detect spondylolysis. n

Back Pain in Young Athletes

Red Flags n n n n n

Systemic illness Radiculopathy Fracture Bowel or bladder dysfunction Neoplasm

Treatment Medical General approach is to stop the activity for 5 to 7 days with gradual return to activity as the pain subsides. n Treatment for spondylolysis includes activity modification and rest. – An antilordotic brace can be used for immobilization in the acute presentation with a 75% healing rate for early defects. n Treatment for hyperlordosis targets mobilization of the thoracolumbar spine, hamstrings, and pelvis; may also consider relative rest or the use of antilordotic bracing. n

Exercises n General strengthening and stretching with emphasis on core abdominal strengthening n Dynamic stabilization exercises targeting the transverse abdominus and multifidi muscles n Sports specific training

Modalities n Heat, cold, ultrasound, and transcutaneous electrical nerve stimulation have been used for symptomatic relief of pain and muscle spasms. Injection Trigger point injections for symptoms of myofascial pain

n

Surgical n Fusion is considered in patients who have continued pain, progression of slippage, neurologic deficits, or a spondylolisthesis of greater than 50%. Consults Physical medicine and rehabilitation n Neurologic or orthopedic-spine surgery n Pediatrics n


Prognosis n

n

The athlete may return to sports, once pain free and range of motion and strength have return to their preinjury baseline. Contact sports are restricted if spondylolisthesis progresses.

Helpful Hints n

Important to balance current athletic performance with future risk of disability

Suggested Reading Sassmannshausen G, Smith BG. Back pain in the young athlete. Clin Sports Med. 2002;21(1):121–132.


Pitfalls Parent’s expectations on the child’s athletic ability and future athletic goals could impair good judgment.

n

43

Brown-Séquard Syndrome Description

n

Charles Edouard Brown-Séquard in 1849 first described a lateral hemisection of the spinal cord affecting the ascending and descending tracts.

n n n n

Etiology/Types

n

Due to compression of the corticospinal tracts resulting in ipsilateral motor, proprioception and vibratory sense deficits, and contralateral pain and temperature sensation deficits n Traditionally associated with knife injuries n Limited number of pure presentations n Brown-Séquard plus syndrome is more common and is often mislabeled as a true Brown-Séquard syndrome. – Described as an asymmetric paresis with hypalgesia, more pronounced on the less paretic side – Both extremities may be paretic

n

n

n n n


n

n

Accounts for 1% to 4% of all traumatic spinal cord injuries (of which there are 11,000 new cases per year) or 40 new cases per million population in the United States Average age of injury is 40 years of age.

Pathogenesis The corticospinal motor fibers cross at the junction of the medulla and spinal cord. – Ascending sensation and vibratory sense fibers found in the dorsal columns remain ipsilateral to the site of entry and then cross over in the medulla. n The spinothalamic tract crosses the midline of the cord one to two segments rostral to the entry level so deficits in pain and temperature usually manifest a few levels below the level of injury. n Loss of ipsilateral autonomic function may also result in a Horner’s syndrome. n


Blunt trauma Cardiac surgery Cervical disc herniations from C2–C3 to C6–C7 Cervical fracture or dislocation related to a fall or motor vehicle accident Epidural hematoma Extramedullary tumors of the spinal cord

44

Acute or gradual onset of symptoms Hemiparesis or hemiparalysis with sensory changes Parasthesias

Natural History n

Epidemiology

Gun shot wound Intravenous drug use Knife wound Local radiation Primary or metastatic tumor Spinal cord herniation Thoracic aortic surgery Transverse myelitis Tuberculosis Vertebral artery dissection

n

Acute or gradual onset Complete or incomplete presentation

Diagnosis Differential diagnosis Acute poliomyelitis n Cervical disc herniation n Guillain-Barré syndrome n Multiple sclerosis n Post-traumatic syringomyelia n

History Injury n Hemiparesis or hemiparalysis with sensory changes n

Exam Findings based on the American Spinal Injury Association (ASIA) impairment scale

n

Testing X-rays are used to assess acute traumatic etiology. n Magnetic resonance imaging (MRI) is useful in assessing damaged soft tissue structures. n

Pitfalls Incorrect SCI diagnosis

n

Red Flags n n

Progressive neurological decline Bowel and bladder dysfunction

Brown-Séquard Syndrome

Medical n Symptomatic treatment Exercises Strengthening and conditioning n Mobility and activities of daily living training n


n

Injection None

n

Prognosis Best prognosis for walking of all spinal cord injuries Complete recovery from Brown-Séquard syndrome following an acute cervical disc herniation was noted in a meta-analysis in 10 of 19 extradural cases versus 3 of 10 intradural cases. n 75% to 90% of patients are able to ambulate independently on discharge from acute rehabilitation. n If the upper limb is weaker than the lower limb, patients are more likely to ambulate on discharge. – In a series of 38 patients published in 1991, patients spent an average of 35 days in acute care and 79 days in intensive rehabilitation. Of these patients, all improved their functional abilities and 29 patients were able to walk independently, 34 had spontaneous bladder emptying, 36 discharged home, 14 were eventually reemployed. n n

Surgical Anterior decompression may provide the safest route in removing intradural disc fragments with the least amount of spinal cord manipulation to allow for improved recovery.

Helpful Hints

Consults Physical medicine and rehabilitation n Neurologic or orthopedic-spine surgery n Neurology

Suggested Readings

n

n

Complications of treatment Progressive spinal cord injury with symptom deterioration n Complications related to surgery n

n

For manifestations related to a cervical disc herniation, prompt evaluation and surgical decompression is important.

McKinley W, Santos K, Meade M, Brooke K. Incidence and outcomes of spinal cord injury clinical syndromes. J Spinal Cord Med. 2007;30(3):215–224. Roth EJ, Park T, Pang T, Yarkony GM, Lee MY. Traumatic cervical Brown-Séquard and Brown-Séquard-plus syndromes: the spectrum of presentations and outcomes. Paraplegia. 1991;29(9):582–589.


Treatment

45

Cauda Equina Syndrome Description

Clinical Features

Cauda equina syndrome results in bowel and bladder dysfunction due to an acute compressive neuropathy of the lumbar and sacral nerve roots.

n

Typically characterized by low back pain, sciatica, saddle and perineal anesthesia, loss of anal tone, loss of bowel or bladder function, and diminished or absent ankle, knee, or bulbocavernous reflexes

Etiology/Types n n n n n n n n n n n n

Trauma Central disc protrusion Intradural and extradural metastasis Ependymomas Schwannomas Neurilemmoma Chiropractic manipulation Inadequate surgical decompression Nerve root swelling Retained disc fragments Hematoma Vascular insufficiency


Overall incidence in the literature is 1% to 5% of spinal pathology. 2% to 6% of lumbar disc herniations can result in cauda equina syndrome. Most common in men in the fourth or fifth decade of life The L4–L5 level is the most commonly involved site followed by the L5–S1 and L3–L4 levels.

Natural History n

Symptoms may develop within several hours or over a longer period of time.

Diagnosis Differential diagnosis n Conus medullaris syndrome n Herniated nucleus pulposus n Lumbar muscle spasm History Deficits with bladder dysfunction are more common than bowel dysfunction. n Bladder dysfunction may manifest as overflow incontinence, incomplete bladder emptying, or marked bladder distension. n Gait dysfunction n

Pathogenesis n

n n

n

The cauda equina consists of the conus medullaris, filum terminale, and motor and sensory nerve roots within the spinal canal. The conus medullaris terminates between the T12 and L2 levels. The nerves supply motor and sensory innervation to the lower extremities and sensation to the perineum, genitalia, and the viscera in the pelvis. Cauda equina syndrome results in a flaccid neurogenic bladder and flaccid external anal sphincter, resulting in overflow incontinence of urine and stool as well as loss of genital sensation, erection, and ejaculation.

Risk Factors n n

Lumbar disc herniation Trauma

46

Sagittal lumbar T2-weighted magnetic resonance image demonstrating a large L4–L5 herniated nucleus pulposus that resulted in a cauda equina syndrome. (Courtesy of Keith Hentel, MD.)

Cauda Equina Syndrome

Testing n MRI or CT may demonstrate a large disc extrusion filling up greater than one third of the central canal diameter. Pitfalls n Sometimes it can be difficult to differentiate between an acute foot drop and a chronic radiculopathy that yields a true cauda equina syndrome.

Red Flags n

Bowel and bladder dysfunction

Treatment Medical Preoperative dexamethasone

n

Exercises Postoperative strengthening and stretching n Postoperative mobility and activities of daily living training n

Modalities n Heat, cold, ultrasound, and transcutaneous electrical nerve stimulation have been used for symptomatic relief of pain and muscle spasms. Injection n None Surgical The goal is decompression within 24 hours

n

n

Laminectomy and discectomy

Consults n Neurologic or orthopedic-spine surgery n Physical medicine and rehabilitation Complications of treatment n Continued bowel, bladder, and motor dysfunction n Complications related to surgery

Prognosis Prognosis is greatly influenced by the preoperative neurologic state. n Surgery within 24 hours allows patients to progress from motor strength of 0–1/5 to 4/5 during the postoperative period. – Patients are normal or near normal within 6 months to 1 year. n With delayed surgery, 58% of patients will have persistent motor deficits. n Motor recovery progresses up to one year n With emergent surgery, three-fourths of patients were discharged from the hospital on intermittent catheterization. By 6 months 95% of patients who underwent emergent surgery had recovered bladder function. n

Helpful Hints n

Immediate surgical consultation with a goal of decompression within 24 hours

Suggested Readings Kennedy JG, Soffe KE, McGrath A, Stephens MM, Walsh MG, McManus F. Predictors of outcome in cauda equina syndrome. Eur Spine J. 1999;8(4):317–322. Shapiro S. Medical realities of cauda equina syndrome secondary to lumbar disc herniation. Spine. 2000;25(3):348–351.


Exam Bilateral sciatica or severe bilateral foot weakness with the inability to stand or walk n Numbness of the perineal region n Decreased or loss of rectal tone n

47

Central Cord Syndrome Description Central cord syndrome was first described by Richard C. Schneider in 1954 as a motor impairment affecting the upper extremities greater than the lower extremities and variable sensory loss below the level of the lesion.

Etiology/Types n

n n

Sudden compression of the cervical spinal cord between the anterior spondylotic disc-osteophyte complex and the thickened posterior ligamentum flavum with hyperextension of the cervical spine in the older population Severe cervical spine trauma in the younger age group Acute cervical disc herniations

Exam Upper-extremity weakness n Bladder dysfunction n Variable sensory loss below the level of the lesion n

Testing MRI can demonstrate increased T2-weighted signal associated with posterior ligamentous injury. n MRI demonstrates hyperintense signal within the parenchyma of the spinal cord at the level of injury. n

Pitfalls Up to 24% of central cord syndrome injuries progress to chronic central cord syndrome, characterized by the delayed development of worsening neurological symptoms, including spasticity.

n

Epidemiology n

Age ranges from 18 to 85 years

Red Flags n

Pathogenesis n

n

Disruption of the medial lamina of the cortical spinal tracts in the central portion of the spinal cord that is responsible for upper-extremity and hand function. Sparing of the lateral tracts that are responsible for lower-extremity function.

Risk Factors n n n

Diving injuries Falls Motor vehicle accidents

Clinical Features n

n

Presentations vary greatly from minor spinal cord trauma that quickly improves with full neurologic recovery to major spinal cord trauma with significant mortality. Bladder dysfunction

Natural History n

Improvement or worsening of symptoms

Diagnosis

Treatment Medical Symptomatic treatment

n

Exercises Strengthening and conditioning n Mobility and activities of daily living training n


n

Injection None

n

Surgical Surgical intervention is not required unless there is spinal instability n Decompressive surgery even after a prolonged nonoperative period may allow for significant improvement if the cause is related to a spondylotic ridge or herniated disc.

n

Consults Neurologic or orthopedic-spine surgery n Physical medicine and rehabilitation

Differential diagnosis n Herniated nucleus pulposus n Other forms of spinal cord injury

n

History n History of trauma, fall, or cervical disc herniation

n

48

Progressive neurologic decline

Complications of treatment Considerable recovery can be achieved using a nonsurgical approach although a progressive neurologic

Central Cord Syndrome

n

decline following recovery and plateau has been noted, which is thought to be due to continued spinal cord compression. Complications related to surgery

n

49

the hands. The return of sensory function does not follow any specific pattern. From 1956 to 1965, out of a total of 42 cases: at discharge, 57% patients were functionally ambulatory and 23% were not ambulatory.

Prognosis

n n

n

Poorer neurologic outcomes correlate with a greater degree of central cervical stenosis. Cord hemorrhage correlates with a more severe injury and limited neurologic recovery. A more favorable outcome is related to a younger age at presentation and no involvement of the lower extremities. Recovery has been described as occurring with motor recovery in the lower extremities followed by improved bladder function. Upper-extremity motor improvement follows next with final improvement in

Helpful Hints n n

Recovery may continue even after discharge, so it is important to continue intensive outpatient rehabilitation. Spasticity influences the ability to ambulate.

Suggested Readings Harrop JS, Sharan A, Ratliff J. Central cord injury: pathophysiology, management, and outcomes. Spine J. 2006;6 (6 Suppl):198S–206S. Roth EJ, Lawler MH, Yarkony GM. Traumatic central cord syndrome: clinical features and functional outcomes. Arch Phys Med Rehabil. 1990;71(1):18–23.


n

Chondrosarcoma Description Chondrosarcoma is a malignant tumor that is made up of a hyaline cartilage matrix and chondrocytes.

Etiology/Types n

Unknown

Epidemiology n n n

n n

Third most common malignant neoplasm after multiple myeloma and osteogenic sarcoma Primarily affects the pelvic and shoulder girdle and is very rare in the axial spine. 9% of patients have lesions affecting the axial spine, of which 50% affect the lumbosacral spine, followed by 32% at the thoracic spine, and 18% at the cervical spine. Usual age of onset ranges from 40 to 60 years. Male predominance

Pathogenesis n n n

Locally aggressive tumor with limited metastatic capability Tumor grows extremely slowly resulting in painless lesions. It may grow to a very large size, especially in the pelvis.


Fibrous dysplasia Irradiation Paget’s disease Preexisting osteochondroma


May present with mild discomfort or pain and a localized palpable swelling Neurologic changes may be the first symptom. Up to 50% of patients have neurologic symptoms.

Natural History n

Tumor grows extremely slowly

Diagnosis Differential diagnosis Chordoma n Giant cell tumor n

50

n

Osteogenic sarcoma

History Mild discomfort n Palpable swelling n Neurologic deficits n

Exam A myelopathic presentation may also develop with invasion or compression of the spinal canal. n Rectal examination may be indicated to assess for pelvic or sacral tumors. n

Testing Laboratory tests include complete blood count, chemistry, and sedimentation rates. n 75% of patients have an abnormal glucose tolerance test with high insulin levels. n X-rays demonstrate a well-defined lesion with expansive contours and a fluffy or lobular interior with scalloping of the inner cortex. n Cortical destruction and soft tissue invasion is a characteristic of aggressive tumors. n CT and MRI allow for delineation of the tumor boundaries in the soft tissue. n CT detects the calcification of the tumor matrix and destruction of the cortical bone and is more reliable for assessing cortical outlines of the bone and mineralized matrix. n MRI allows for delineation of tumor penetration into the bone marrow, soft tissue, and spinal canal. n MRI demonstrates high signal intensity on T2-weighted images, which is thought to be caused by the high water content of the hyaline cartilage. n Higher grade lesions demonstrate increased diffuse or nodular contrast enhancement. n A bone scan may detect metastatic lesions. n Biopsy confirms the diagnosis. n Arteriography is useful for detecting major feeding vessels, which can help in surgical planning as well as determining the overall extraosseous involvement. n

Pitfalls Chondrosarcoma with new onset of pain suggests active growth.

n

Red Flags n

Myelopathy

Chondrosarcoma

Medical n No chemotherapeutic agents have been found to be helpful. Exercises None

Consults n Neurologic or orthopedic-spine surgery Complications of treatment n Surgical complications from an en bloc excision n Progressive neurologic dysfunction

n

Prognosis

Modalities n None

n

Injection None

Helpful Hints

n

Surgical Laminectomy or decompression allows for transient improvement in neurologic symptoms. n En bloc surgical excision with wide histologic margins without contaminating the site with neoplastic cells offers the best chance for a complete cure, although can be technically difficult. n

n

One study found that 50% of patients with contaminated margins died after local recurrence

Surgery can be technically difficult, and the extent of the resection impacts the recurrence rate and functional rehabilitation.

Suggested Readings Camins MB, Duncan AW, Smith J, Marcove RC. Chondrosarcoma of the spine. Spine. 1978;3(3):202–209. Shives TC, McLeod RA, Unni KK, Schray MF. Chondrosarcoma of the spine. J Bone Joint Surg Am. 1989;71(8):1158–1165.


Treatment

51

Chordoma Description

n

Chordoma is a low-grade malignancy arising from the embryonic notochord cells in the spine.

n n n

Etiology/Types n

Unknown

n n n


Accounts for 3% to 4% of primary bone tumors 50% are found in the sacrococcygeal region. 35% occur in the basioccipital region. Skull-based presentations occur in adolescents and children. Most common in the fifth and sixth decade Male to female ratio 2:1

Pathogenesis n

Physaliphorous cells with glycogen and oxidative enzyme-filled vacuoles of notochord origin are a distinct feature.

n n

Chondrosarcoma Giant cell tumor Intrasacral cysts Metastases Multiple myeloma Osteoblastoma Osteochondroma Osteosarcoma Teratoma

History n Vague symptoms due to local compression Exam Cervical spine presentation may result in unilateral paresthesias or weakness n Sacral presentation may be detected by a rectal examination as a firm, round mass on the posterior wall of the rectum n Spasticity is noted with high lumbar presentations whereas sacral presentations may present with decreased tone. n

Risk Factors n

Trauma

Clinical Features n n n n n n n

Vague symptoms due to local compression as the tumor enlarges Symptoms related to compression of neural elements and pressure on the pelvic structures Referred pain to the hip, groin, knee, or sacroiliac joint Night pain Pain not relieved with recumbency Cervical spine presentation may result in unilateral paresthesias or weakness Progressive dyspnea if the tumor is located in the cervicothoracic region.

Natural History n n

Slow, clinical course Mainly remains local but may metastasize to the lungs, bone, and liver.

Diagnosis Differential diagnosis Aneurysmal bone cyst

n

52

Sagittal lumbosacral T1-weighted magnetic resonance image of a chordoma that has grown into the pelvis, forward displacing the rectum. (Adapted from Fast A, Goldsher D. Navigating the Adult Spine: Bridging Clinical Practice and Neuroradiology. New York: Demos Medical Publishing, 2007:111.)

Chordoma

Pitfalls Diagnosis is usually late

n

Injection n None Surgical n En bloc excision or high sacral amputation is the preferred method of treatment, although the patient may lose normal bowel and bladder function. n Tumor spillage may increase the local recurrence rate from 28% to 64%. n Surgery is limited by technical constraints and quality of life issues. Consults Neurologic or orthopedic-spine surgery n Physical medicine and rehabilitation n

Complications of treatment n Sacral resections above the S2 level result in significant perioperative morbidity and long-term problems. n Surgical complications from an en bloc excision

Prognosis n

Red Flags n n

Progressive dyspnea Unstable spine

n n

Treatment Medical Radiation therapy is indicated if a complete excision cannot be done and it may slow tumor growth and increase the survival rate. n Local control at 5 years with proton beam radiation therapy is 50% to 60%. n

Exercises n None Modalities n None

Prognosis should be based on location, pathology, and invasiveness. 5-year survival rates have been reported to be 86% with local recurrence free survival of 60%. Local failure rate with a marginal resection can be greater than 70%.

Helpful Hints n n

Local recurrences are frequent En bloc excision or high sacral amputation is the preferred method of treatment.

Suggested Readings Casali PG, Stacchiotti S, Sangalli C, Olmi P, Gronchi A. Chordoma. Curr Opin Oncol. 2007;19(4):367–370. York JE, Kaczaraj A, Abi-Said D, et al. Sacral chordoma: 40-year experience at a major cancer center. Neurosurgery. 1999;44(1):74–79; discussion 79–80.


Testing The tumor appears as a well-encapsulated, lobulated, soft grayish mass on gross examination. n X-rays demonstrate destruction of several segments of the axial or sacral spine with a characteristic appearance of a soft tissue mass with lytic bony destruction and calcified foci. n A bone scan usually does not show increased uptake at the site. n CT scan can demonstrate the extent of bony involvement. n Myelography may miss a sacral presentation as the sacral canal ends at the S2 level n MRI is useful in staging and diagnosing these lesions based on increased T2-weighted signal compared to the adjacent soft tissues. n Biopsy is used for definitive diagnosis. n Sacral chordomas frequently require an open biopsy. n

53

Coccydynia (Coccygodynia) Description Coccydynia is pain due to an injury of or originating from the coccyx.


Associated with obesity, which decreases pelvic rotation with sitting Trauma, including falls Challenging vaginal delivery that results in subluxation

Epidemiology n n

Mean age of onset is 40 years Female to male ratio of 5:1

Pathogenesis n

n

n

n

Sacrum consists of five fused sacral bones followed by the coccyx, which is a triangular structure made up of three to four fused coccygeal vertebrae. Sacral cornu (S5), articulates with the coccygeal cornu via a zygapophyseal (facet) joint disc complex, which can be a symphysis or a synovial joint. Coccyx also provides anchor points for the origin of the coccygeal and gluteus maximus muscles as well as the anococcygeal ligaments. Mobility of the segments and their angulation do not appear to increase the risk of pain.

Risk Factors n n

Immobile coccyx may result in the formation of a bursitis at the tip. Obesity


History of a fall or chronic insidious pain in the buttock Worsened with sitting or arising from a seated position, bowel movements, or walking Improved with offloading the coccygeal area by shifting weight on either buttock or onto the legs Point tenderness at the sacrococcygeal region with associated muscle spasm on rectal examination

Natural History n

Episodic or continuous, unrelenting, mild to debilitating pain

54

Diagnosis Differential diagnosis n Arachnoiditis n Coccyx and sacral tumors n Coccyx dislocation or fracture n Lumbar intervertebral disc disease n Perirectal abscesses n Pilonidal cysts n Posttraumatic arthritis of the sacrococcygeal joint History History of a fall or worsening buttock pain

n

Exam Assess for bruising or erythema related to acute trauma n Assess for pilonidal cysts or fistulas n Point tenderness at the sacrococcygeal region or the location of trauma n No tenderness in the adjacent musculature or soft tissue n Palpate for edema, masses, or bony spicules in the surrounding tissue or intrarectally n Decreased, increased, or normal coccygeal flexibility n Reproduction of pain with coccygeal motion n Intrarectal manipulation may demonstrate similar findings with adjacent musculature muscle spasm. n

Testing Lateral X-rays of the coccyx with normal sitting and standing demonstrates a coccygeal pivot of 5 to 25 degrees anteriorly or posteriorly with sitting, returning to the normal position with standing. n Coccyx in symptomatic patients pivots anteriorly >25 degrees or subluxes posteriorly with sitting. n MRI may demonstrate increased T2 signal at the hypermobile or subluxed segment. n Technetium Tc-99m bone scan may demonstrate increased activity at the hypermobile or subluxed segment. n

Pitfalls Often takes years for a firm diagnosis n May impact academic or vocational performance n Acute presentations may be very debilitating n

Red Flags n

Important to rule out a metastasis or tumor if the patient notes blood during defecation

Coccydynia

Medical n Short-term NSAIDs n Muscle relaxants n Analgesics n Hot baths n Cushion Exercises Pelvic floor strengthening especially following pregnancy

n

Modalities 16% of patients improved with 2 weeks of ultrasound followed by 2 weeks of diathermy. n Manipulation is thought to relax intrapelvic muscle tension of the levator ani, coccygeus, and piriformis muscles. n One study demonstrated that three to four sessions of levator anus massage and stretching were more effective than joint mobilization alone, and those patients with an immobile coccyx fared worse than patients with a mobile coccyx. n

Injection n Diagnostic block with local anesthetic may also be helpful in diagnosing a hypermobile or subluxed segment. n Steroid infiltration of the sides and tip of the coccyx may be helpful. n Repeated flexion and extension of the coccyx for one minute under general anesthesia may be helpful.

n

Fluoroscopically guided ganglion impar blocks via the sacrococcygeal junction or first intracoccygeal junction

Surgical Surgical indications include disabling coccyx pain with radiographic signs of subluxation, instability, or a bone spur n Coccygectomy demonstrates a 60% to 91% success rate. n

Consults Orthopedic-spine surgery n Physical medicine and rehabilitation n

Complications of treatment n Surgical complications include wound infection ranging from 2% to 22%.

Prognosis n

Good outcomes noted with nonsurgical and surgical treatments.

Helpful Hints n

Often chronic pain which takes years for a firm diagnosis

Suggested Readings Foye PM, Buttaci CJ, Stitik TP, Yonclas PP. Successful injection for coccyx pain. Am J Phys Med Rehabil. 2006;85(9):783–784. Wray CC, Easom S, Hoskinson J. Coccydynia: aetiology and treatment. J Bone Joint Surg Br. 1991;73:335–338.


Treatment

55

Deconditioning Description

Risk Factors

Deconditioning should be considered a separate condition from the original illness.

n

Etiology/Types n

Loss of normal physiological load on tissues

Epidemiology n n

Common in hospitalized patients or other situations of significantly decreased activity More common in the older population

n


Pathogenesis n

n n

n

n

n

n n

n n

Horizontal positioning reduces energy consumption and increases the chances of surviving a medical crisis, but also accelerates the process of deconditioning. Peak aerobic capacity can be reduced by up to 31% after 30 days of bed rest. The change in VO2max is based on the premorbid level of aerobic conditioning and the duration of bed rest, but is not affected by age or gender. The physiological mechanisms responsible for deconditioning include decreased maximal stroke volume and cardiac output; decreased venous return caused by lower blood volume; and decreased pulmonary capacity. Muscle weakening is thought to be related to the loss of muscle mass and changes in motor control, contractile properties, electromechanical coupling, and decreased nerve conduction. Three weeks of inactivity in the peripheral joints can cause an alteration in tendon stiffness and increase bone turnover, resulting in an increased risk of sprains and fractures during the rehabilitation process 9% loss of muscle mass in the multifidus and erector spinae with only a few weeks of horizontal bed rest Patients without a history of low back pain who are required to remain in bed for prolonged periods of time may compromise the function of their multifidus muscles, predisposing them to future lower back pain. Overall, may lose up to 1% to 1.5% of muscle strength per day. Prolonged immobility may result in a loss of 25% to 40% of muscle strength.

56

Chronic prolonged illness Immobility

Based on primary illness and the premorbid level of conditioning Significant muscle wasting Poor endurance Joint contractures Loss of strength is greater in the proximal muscles compared with the distal muscles.

Natural History n

Progressive worsening with decreased activity

Diagnosis Differential diagnosis n Cardiopulmonary disease n Connective tissue disease n Critical illness polyneuropathy n Multiple sclerosis n Neuropathy n Steroid myopathy History Generalized weakness n Decreased endurance n

Exam Muscle wasting n Joint contractures n Difficulty with functional tasks n

Testing Electrodiagnostic studies may demonstrate decreased motor unit action potentials and/or denervation with severe wasting.

n

Pitfalls n Overlooked treatable underlying diagnosis

Red Flags n

Progressive myopathy or neuropathy

Treatment Medical Proper nutrition to support muscle development

n

Deconditioning

57

Exercises Patients with 2 weeks of bed rest will not return to their pre–bed rest cardiovascular response even after 3 weeks of ambulation and mild exercise. n Severe deconditioning requires a period of immobilization three times as long as the initial requirement in order to regain lost strength. n Minimal daily isometrics exercises can significantly decrease the progression. n Strengthening and conditioning n Stretching n Neuromuscular reeducation and coordination n Proprioception and balance exercises n Mobility and activities of daily living training

Consults n Nutrition n Geriatrics in the older patient population

Modalities n Heat, cold, ultrasound, and transcutaneous electrical nerve stimulation have been used for symptomatic relief of pain and muscle spasms.

Helpful Hints

Injection n None

Bloomfield SA. Changes in musculoskeletal structure and function with prolonged bed rest. Med Sci Sports Exerc. 1997;29(2):197–206. Rader MC, Vaughen JL. Management of the frail and deconditioned patient. South Med J. 1994;87(5):S61–S65.

Surgical None

n

Complications of treatment n Muscle strains or sprains n Tendonopathies n Pain from reconditioning program n Increased risk of fracture, especially in osteopenic or osteoporotic patients

Prognosis n n

n

Generally good to excellent Overall based on underlying health status

Patients have to understand that reconditioning is a long, slow process.

Suggested Readings


n

Diffuse Idiopathic Skeletal Hyperostosis (Forrestier’s Disease) Description

n

Diffuse idiopathic skeletal hyperostosis (DISH) manifests as axial spine stiffness and pain and is characterized by calcification of the spinal and the adjacent extraspinal structures on plain radiographs.

Diagnosis

Potential development of cervical myelopathy, spinal cord injury, and dysphagia

Differential diagnosis Acromegaly n Hypoparathyroidism n Neuropathic arthropathy n Ochronosis n Spondyloarthropathies n Trauma n


Generally unknown etiology Possibly related to occupational stress and trauma Insulin and retinoic acid may play a role as they may act as bone growth factors


Common in men aged 48 to 85 years Male to female ratio is 2:1 Most common in whites, Asians, and Native Americans Found in 6% to 28% of autopsies

Pathogenesis n

Calcification and ossification occur in soft tissues, particularly the ligaments and entheses.

Risk Factors n

Unknown


n n

57% of patients initially complain of thoracolumbar back pain. 50% of patients report neck pain. 80% of affected individuals complain of spinal stiffness 10 to 20 years before diagnosis. Right-sided preference in the axial spine Mild to severe dysphagia occurs in 17% to 28% of patients with anterior osteophytes in the cervical spine. 37% of patients have extraspinal enthesopathies in the peripatellar ligaments, plantar fascia, olecranon, and the Achilles tendons. 50% of patients with DISH also have ossification of the posterior longitudinal ligament (OPLL). Associated with ossification of the ligamentum flavum

History Stiffness improves during the day n Stiffness worse in the morning and evening n Stiffness worsens with immobility n

Exam Decreased cervical and lumbar lordosis n Affected extraspinal joints may demonstrate decreased range of motion. n Normal axial spine range of motion is preserved because the posterior elements do not fuse. n

Testing Diagnosis is based on radiographic findings using Resnick and Niwayama’s criteria. n Recognized on X-rays by flowing ossification along the anterolateral vertebrae of at least four contiguous vertebrae with the absence of a spondyloarthropathy or degenerative changes. n X-ray findings include the absence of sacroiliac joint sclerosis, erosion, or fusion; preservation of disc heights without evidence of degenerative disc disease; absence of apophyseal joint bony ankylosis. n Thoracic and L1–L3 lumbar involvement are the most common findings. n C4–C7 segments are the most commonly affected vertebrae in the cervical spine. n MRI is useful in locating suspected fractures in the vertebral bodies, based on intervertebral fluid collections or assessing for OPLL. n

Pitfalls Spinal fractures in older patients may be missed or delayed in diagnosis due to their baseline pain with an increased risk of neurologic sequelae with spinal instability.

n

Natural History n

Progressive axial spine stiffness and pain

58

Diffuse Idiopathic Skeletal Hyperostosis

59

Treatment Medical n Focus on pain relief and maximizing function n NSAIDs for pain control Exercises n General strengthening and stretching n Home exercise programs focus on maintaining axial spine flexibility Modalities Heat, cold, ultrasound, and transcutaneous electrical nerve stimulation have been used for symptomatic relief of pain and muscle spasms. Injection Trigger point injections for symptoms of myofascial pain

n

Surgical Surgery may be considered in patients with dysphagia associated with anterior cervical osteophytes although recurrence is possible.

n

Consults Neurologic or orthopedic-spine surgery n Physical medicine and rehabilitation n

Complications of treatment n Variable Anterioposterior AP thoracic plain radiograph demonstrating flowing osteophytes bridging greater than four vertebral bodies (arrow) in a patient with diffuse idiopathic skeletal hyperostosis. (Adapted from Fast A, Goldsher D. Navigating the Adult Spine: Bridging Clinical Practice and Neuroradiology. New York: Demos Medical Publishing, 2007:82.)

Red Flags n

Neurologic compromise from spinal cord impingement or dysphagia from cervical spine involvement

Prognosis n

Benign course

Helpful Hints n

Assess for spinal fractures in older patients

Suggested Reading Sarzi-Puttini P, Atzeni F. New developments in our understanding of DISH (diffuse idiopathic skeletal hyperostosis). Curr Opin Rheumatol. 2004;16(3):287–292.


n

Disciitis Description

n

Disciitis is an infection of the intervertebral disc space.

Etiology/Types n n

Osteomyelitis Hematogenous spread and direct inoculation during an interventional procedure or surgery

The pain may radiate to the upper extremities and hands if originating from the cervical spine or the abdomen, flanks and lower extremities if originating from the thoracic or lumbar spine.

Natural History n

Progressively worsening pain and disability over 2 years before a diagnosis is confirmed.


Uncommon in adults Reported in patients into the sixth decade 2.8% develop an infection following lumbar disc surgery Male predominance

Pathogenesis n n n n n n

Hematogenous spread is considered the route of entry in children. Lumbar spine is affected in 77% of cases, the cervical spine in 15%, and the thoracic spine in 8%. Gram-positive organisms include Staphylococcus aureus, Streptococcus epidermidis, and Streptococcus milleri. Gram-negative organisms include Pseudomonas aeruginosa, Escherichia coli, and Campylobacter fetus. Fungal organisms include Aspergillus fumigatus. Biopsy specimens may demonstrate cellular necrosis and adjacent vertebral osteomyelitis.

Risk Factors n n n n n n n n n n n n n

Absent prophylactic antibiotic coverage prior to an invasive procedure Adjacent abscess Cerebral angiography Debilitated patients Diabetes Discography Epidural anesthesia during delivery Fracture Heavy physical labor Immunocompromised patients Needle biopsy of the intervertebral disc Operative procedures Trauma

Clinical Features n

Localized spinal pain ranging from mild and insidious to acute and severe

60

Diagnosis Differential diagnosis Calcium pyrophosphate dehydrate crystal deposition n Chordoma n Degenerative disc disease n Myeloma n Osteomyelitis of the vertebral body n Spinal erosive changes associated with chronic renal failure n Trauma n

History Sharp, severe pain n Pain may be referred to the extremities n Pain worsens with movement, improved with rest n A period of postsurgical improvement followed by worsening pain n Preference for recumbency n

Exam Fever is rare n Localized tenderness to palpation n Limited axial spine range of motion n Neurologic deficits that suggest myelopathy or spinal cord compression n

Testing Elevated erythrocyte sedimentation rate, C-reactive protein, and leukocytosis n Blood cultures may be positive n Culture of the infectious fluid or tissue may be positive n Plain radiographs may demonstrate loss of disc height, adjacent reactive sclerosis of the subchondral bone, irregularity of the end plates. n Bone scan may demonstrate increased bony activity within the adjacent vertebral bodies. n CT can demonstrate disc space narrowing and erosion through the endplate n MRI can detect changes before plain radiographs. n

Disciitis n n

61

Bracing Bed rest

Exercises n None Modalities n Modalities are contraindicated as they may increase the spread of the infectious process. Injection None

Surgical n Surgery is reserved for spinal instability, deformity, and cord compression. n CT–guided percutaneous drainage n Surgical fusion is usually unnecessary.

Sagittal lumbar T2-weighted magnetic resonance image with fat suppression demonstrating intervertebral disc destruction and progressive involvement of the adjacent vertebral bodies associated with disciitis. (Courtesy of Keith Hentel, MD.)

Consults n Neurologic or orthopedic-spine surgery n Infectious disease Complications of treatment n Complications related to surgery include hemiplegia and tetraplegia.

Prognosis Pitfalls n Diagnostic delay

n n

Red Flags n

Associated radiculopathy or paraparesis

The prognosis in children is good, as arterioles supply the developing end plates in children. Antibiotics given early can limit the extent of intervertebral disc and vertebral body destruction.

Helpful Hints Early identification and treatment is crucial.

Treatment

n

Medical A 4- to 6-week course of antibiotics n Immobilization

Suggested Reading

n

Schulitz KP, Assheuer J. Discitis after procedures on the intervertebral disc. Spine. 1994;19(10):1172–1177.


n

Ehlers–Danlos Syndrome Description

n

Ehlers–Danlos syndrome (EDS) is a rare hereditary collagen metabolism disorder resulting in joint and soft tissue hypermobility.

n

Natural History n

Etiology/Types n n n n n n

Classic Hypermobile Vascular Kyphoscoliosis Arthrochalasia Dermatosparaxis

Epidemiology n

Estimated incidence is 1 in 5,000 live births.

Pathogenesis n n

Mutations affect type I and III procollagen or enzymes that modify collagen. Defect in the formation of collagen fibrils

Risk Factors n

Hereditary

Clinical Features n n n n n n n n n n n n n n n n n n

Joint hypermobility with possible subluxation or dislocation Skin hyperextensibility and fragility Friable soft tissues with easy bruising and poor healing Kyphoscoliosis is common in type IV EDS. Pigmented scars over the bony prominences of the epicanthal folds, forehead, and chin Blue sclera Wide-set eyes Thin cheek bones “Lobeless” ears Patients may be able to touch the tip of their nose with their tongue Weak collapsible handclasp Pes planus Early osteoarthritis Shoulder laxity and instability Soft velvety skin Poor vision Mitral valve prolapse Aortic aneurysm

62

Obstetric or gynecologic complications Increased risk of Chiari I malformation

n n

Hypermobility causes back pain in 6% to 67% of affected individuals. Spinal deformity is most common in the arthrochalasia, kyphoscoliosis, and classic types. Spondylosis or spondylolysis may also develop due to tissue laxity.

Diagnosis Differential diagnosis Marfan syndrome n Osteogenesis imperfecta n Other collagen vascular disorders n

History Back pain n Kyphoscoliosis n

Exam Joint hypermobility n Skin hyperextensibility and fragility n Friable soft tissues with easy bruising and poor healing n Hypermobile spine n Spinal deformity n Assessed using the Beighton scale (Carter–Wilkinson criteria) n

Testing Plain radiographs demonstrate kyphoscoliosis at the thoracolumbar junction with anterior wedging and posterior scalloping of the vertebral bodies.

n

Pitfalls Osteoporosis

n

Red Flags n n

Vascular injuries such as bleeding or compartment syndrome Sciatic neuropathy

Treatment Medical Nonoperative treatment preferred n Brace trial during adolescent growth stage may prevent the formation of scoliosis. n

Ehlers–Danlos Syndrome

Education regarding behavior modifications, proper ergonomics, and posture is very important.

Exercises Strengthening and proprioception exercises n General strengthening and stretching with emphasis on core abdominal strengthening n Low impact aerobic exercise such as swimming n


n

Injection n Trigger point injections and epidural injections may be done for symptomatic relief and should be done with caution due to vessel friability and poor wound healing potential. Surgical Fusion for progressive spine deformity

n

Consults Physical medicine and rehabilitation n Rheumatology n

n

Neurologic or orthopedic-spine surgery for spinal instability

Complications of treatment Surgical complications include poor healing potential, wound dehiscence, paraplegia, radiculopathy, vascular injury, and abnormal scar formation due to abnormal tissue resilience.

n

Prognosis n

Unknown

Helpful Hints n

Education regarding behavior modifications, proper ergonomics, and posture is very important.

Suggested Readings Akpinar S, Gogus A, Talu U, Hamzaoglu A, Dikici F. Surgical management of the spinal deformity in Ehlers-Danlos syndrome type VI. Eur Spine J. 2003;12(2):135–140. McMaster MJ. Spinal deformity in Ehlers-Danlos syndrome. Five patients treated by spinal fusion. J Bone Joint Surg Br. 1994;76(5):773–777. Schroeder EL, Lavallee ME. Ehlers-Danlos syndrome in athletes. Curr Sports Med Rep. 2006;5(6):327–334.


n

63

Epidural Abscess Description

n

An epidural abscess is a rare medical emergency that may result in severe and irreversible neurologic deficits.

n

Etiology/Types

n

n n n n n n n n

66% of cases are due to Staphylococcus aureus. Increasing incidence of methicillin-resistant S. aureus (MRSA) Staphylococci epidermidis Escherichia coli Pseudomonas aeruginosa Fungi Mycobacteria Parasites

Epidemiology n n

1 in 10,000 hospital admissions Male predominance


Contiguous (33%) or hematogenous (50%) spread Direct compression or vascular occlusion (septic thrombophlebitis) of the spinal cord Usually extends over three to four spinal segments Osteomyelitis is associated with 80% of epidural abscesses.

Risk Factors n n n n n n n n n n n n n n

Alcoholism Catheter or stimulator placement Degenerative joint disease Diabetes mellitus Epidural analgesia HIV Increasing age Injection-drug use Nerve blocks Sepsis Skin or soft tissue infection Spinal instrumentation Trauma Urinary tract infection


Stage 1: Acute onset, severe neck, or back pain at the affected level (75% of patients) Stage 2: Progressive radicular pain

64

Stage 3: Motor and sensory dysfunction with bowel and bladder dysfunction (33% of patients) Stage 4: Spinal cord compressive injury or infarction resulting in paralysis affects 4% to 22% of patients Fever (50% of patients)

Natural History n

Progressive constitutional illness and back pain with progressive neurologic dysfunction and paralysis leading occasionally to death

Diagnosis Differential diagnosis Discitis n Endocarditis n Osteomyelitis n Sepsis n Spinal hematoma n Transverse myelitis n Urinary tract infection n

History Acute onset n Severe neck or back pain n Progressive neurologic deficit n

Exam Disorientation n Fever n Progressive neurologic deficit n Bowel or bladder dysfunction n

Testing Elevated erythrocyte sedimentation rate, C-reactive protein, and leukocytosis n Bacteremia is present in 60% of cases. n CSF analysis demonstrates increased protein and pleocytosis. n X-rays may demonstrate disk space narrowing or bone lysis but is not useful in 20% of cases. n MRI with intravenous gadolinium contrast n CT-guided needle aspiration n Bone scan may show increased uptake. n

Pitfalls 11% to 75% of cases are misdiagnosed. n The classic triad of back pain, neurologic dysfunction, and fever is not common. n

Epidural Abscess

n

65

neurologic compromise can occur with appropriate antibiotics. Intravenous antibiotic treatment for 6 weeks due to the coexistence of osteomyelitis

Exercises None

n

Modalities n Modalities are contraindicated as they may increase the spread of the infectious process. Injection None

Surgical n Decompressive laminectomy with debridement is done urgently due to the unknown rate of progression.

Sagittal thoracic T2-weighted magnetic resonance image demonstrating a hyperintense mass dorsal to the spinal cord (arrow) characteristic of an epidural abscess. (Adapted from Fast A, Goldsher D. Navigating the Adult Spine: Bridging Clinical Practice and Neuroradiology. New York: Demos Medical Publishing, 2007:66.)

Consults Infectious disease n Neurologic or orthopedic-spine surgery n

Complications of treatment n Persistent neurologic dysfunction

Prognosis n

Red Flags n

Progressive neurologic decline

n

Preoperative neurologic status immediately before surgery is the best predictor of final neurologic outcome. Patients with paralysis of >24 to 36 hours may gain some neurologic function up to one year. 5% to 16% mortality rate

Treatment

n

Medical Empiric antibiotics against S. aureus with vancomycin to cover for MRSA and a third- or fourth-generation cephalosporin to cover for gram-negative bacilli should be used while cultures are pending. n Systemic antibiotics can be used alone in patients with little or no neurologic compromise, although

Helpful Hints

n

n

The classic triad of back pain, neurologic dysfunction, and fever is not common.

Suggested Reading Darouiche RO. Spinal epidural abscess. N Engl J Med. 2006;355(19):2012–2020.


n

Epidural Lipomatosis Description

Natural History

Epidural lipomatosis is the accumulation of normal fatty tissue in the extradural space encroaching on the spinal canal and compressing the neural elements that results in neurologic dysfunction.

n n

Unknown May occur 6 months to 13 years after the beginning of corticosteroid medication

Diagnosis Etiology/Types n

Unknown


More common in the thoracic spine followed by the lumbar spine Never reported in the cervical spine Male predominance Mean age of onset is 43 years, although it has been described in a 6-year-old undergoing exogenous corticosteroid therapy.

Pathogenesis n

The spinal cord and nerve roots are slowly compressed.

Differential diagnosis n Arteriovenous malformation n Collagen vascular disease n Epidural hematoma n Epidural abscess n Heavy metal poisoning n Neoplasm n Peripheral neuropathy or myopathy related to medication or diabetes n Porphyria n Vertebral body compression fracture related to osteoporosis History Back pain

n

Risk Factors n n n n n n n n n n n n n n

Asthma Anabolic steroid use Cushing’s disease Epidural steroid injections Exogenous corticosteroid therapy ranging from 5 to 180 mg per day (most common) Hypothyoidism Idiopathic Inhaled steroids Morbid obesity Pituitary prolactinoma Polyarteritis nodosa Radiation pneumonitis Renal transplants Rheumatoid arthritis


Back pain is the most common symptom. Lower-extremity motor and sensory deficits Upper or lower motor neuron signs Decreased proprioception Sphincter dysfunction

66

Sagittal lumbar T1-weighted magnetic resonance image demonstrating dural sac compression at L4 and below (arrow) caused by fatty tissue in epidural lipomatosis. (Adapted from Fast A, Goldsher D. Navigating the Adult Spine: Bridging Clinical Practice and Neuroradiology. New York: Demos Medical Publishing, 2007:52.)

Epidural Lipomatosis

n n

Weakness Sensory loss Burning dysesthesias

Exam Upper or lower motor neuron signs n Positive straight leg raise n

Testing Workup to assess for overproduction of endogenous corticosteroid in idiopathic cases n MRI demonstrates increased T1-weighted signal and intermediate T2-weighted signal in the lipid mass. n CT can be used to demonstrate soft tissue surrounding the thecal sac. n

Pitfalls Subclinical lumbar stenosis due to degeneration versus epidural lipomatosis in older patients

n

Red Flags n n

Cauda equina syndrome Progressive lower-extremity weakness

Treatment Medical n Discontinuation of corticosteroid therapy n Weight reduction in obese patients Exercises n None Modalities Heat, cold, ultrasound, and transcutaneous electrical nerve stimulation have been used for symptomatic relief of pain and muscle spasms.

n

Injection None

n

Surgical n Laminectomy with epidural adipose tissue resection is required for cauda equina syndrome or spinal cord compression. Consults Physical medicine and rehabilitation n Neurologic or orthopedic spine surgery n

Complications of treatment n Increased mortality with laminectomies in patients requiring high-dose corticosteroid therapy

Prognosis n

n

n

n

Epidural fatty tissue may disappear with associated resolution of symptoms following discontinuation of exogenous corticosteroid therapy. Outcomes of surgical decompression in the lumbar region tend to be more successful compared to the thoracic region. 22% mortality rate within one year in one study due to significant comorbidities in patients who have had laminectomies Recurrence of fatty tissue is rare.

Helpful Hints n

Obese patients may respond to a conservative weightloss approach.

Suggested Readings Fassett DR, Schmidt MH. Spinal epidural lipomatosis: a review of its causes and recommendations for treatment. Neurosurg Focus. 2004;16(4):E11. Fessler RG, Johnson DL, Brown FD, Erickson RK, Reid SA, Kranzler L. Epidural lipomatosis in steroid-treated patients. Spine. 1992;17(2):183–188. Ishikawa Y, Shimada Y, Miyakoshi N, et al. Decompression of idiopathic lumbar epidural lipomatosis: diagnostic magnetic resonance imaging evaluation and review of the literature. J Neurosurg Spine. 2006;4(1):24–30.


n

67

Ewing’s Sarcoma Description Ewing’s sarcoma is a malignant round cell tumor of bone and soft tissue primarily affecting children and adolescents.

Etiology/Types n

Most cases are characterized by a t(11;22)(q24;q12) balanced translocation.

Epidemiology n n n n n

Second most common malignant primary bone tumor in children and adolescents Typical age of presentation is 12 to 24 years. Male to female ratio of 2:1 3.5% occur in the axial spine Most common sites of occurrence are the pelvis, tibia, fibula, and femur.

Pathogenesis n n n

Primary malignant sarcoma Uniform small blue round cells noted with microscopy Grossly it is grayish white and soft.

Risk Factors n

Unknown


Typically presents as local pain, palpable mass, and neurologic deficits Low back pain is usually the first symptom. 58% of patients have neurologic deficits. Possible overlying point tenderness on the axial spine

Natural History n

Increased local pain and progressive neurologic deficits

Diagnosis Differential diagnosis Malignant lymphoma n Neuroblastoma n Primitive neuroectodermal tumor of bone n Rhabdomyosarcoma n

History n Low back pain

68

n

Neurologic dysfunction

Exam n Palpable mass n Neurologic deficits Testing Light microscopy n Immunohistochemical and possibly cytogenetic analysis n X-rays are normal initially but eventually demonstrate vertebral lytic bone destruction. n MRI allows for early detection and allows for understanding the extent of soft tissue involvement, including the epidural space and extension into the bone marrow. n The tumor demonstrates decreased signal on T1-weighted images. n CT assesses the extent of bony involvement, as well as outlines the extent of soft tissue involvement. n Large bore needle biopsy should be done rather than an open biopsy through a laminectomy, as this decreases the risk of postlaminectomy kyphosis. n Bone scan can be used to assess for systemic disease. n

Pitfalls Progressive neurologic dysfunction

n

Red Flags n

Neurologic deficits

Treatment Medical Radiation n Chemotherapy regimens include vincristine, actinomycin, and cyclophosphamide with or without adriamycin. n

Exercises None

n

Modalities None

n

Injection None

n

Surgical En bloc spondylectomy should be considered if there is no evidence of metastasis as long-term survival may be increased.

n

Ewing’s Sarcoma

Consults Neurologic or orthopedic-spine surgery

n

Prognosis n

Long-term disease-free survival rates with either surgery or radiation ranges from 5% to 20 %, but with

n

n

chemotherapy along with radiation or surgery the survival rate jumps to 50% to 80%. Recurrence rates following chemotherapy and radiation therapy range from 15% to 21%, although this is expected to be lower following en bloc resection. Death results from widespread hematogenous spread.

Helpful Hints n

En bloc spondylectomy within the axial spine can be very challenging.

Suggested Readings Grubb MR, Currier BL, Pritchard DJ, Ebersold MJ. Primary Ewing’s sarcoma of the spine. Spine. 1994;19(3):309–313. Marco RA, Gentry JB, Rhines LD, et al. Ewing’s sarcoma of the mobile spine. Spine. 2005;30(7):769–773.


Complications of treatment n En bloc spondylectomy within the axial spine can be very challenging. n Radiation-associated sarcoma and myelopathy n Postlaminectomy kyphosis is the most common complication, which can lead to progressive kyphosis and eventual neurologic compromise. – Caused by loss of the posterior tension band following a decompressive laminectomy, which can result in spinal instability. – Risk decreased with spinal stabilization

69

Failed Back Surgery Syndrome Description Failed back surgery syndrome describes continued pain following one or more spinal surgeries. The term is controversial as some believe it is not a diagnosis.

Etiology/Types n

Multiple spine surgeries

Epidemiology n

n

Approximately 2,000 cases of failed back surgery syndrome are produced yearly in the United Kingdom. Typically involves younger patients.

Pathogenesis n

Variable


Anxiety Depression Inability to achieve surgical goal and continued progressive disease Inappropriate surgical procedure Incorrect diagnosis Litigation Number of previous surgeries Poor patient selection Poor surgical technique Worker’s compensation payments

Clinical Features n

n n n n n

Pain following surgery suggests the disc may not have been adequately decompressed or the wrong level was chosen 1 to 6 months of pain-free status suggests the development of arachnoiditis or infection. Greater than 6 months of pain-free status suggests a recurrent disc herniation. Leg and back pain suggests arachnoiditis or spinal stenosis. Spinal stenosis and scar tissue can coexist. Arachnoiditis usually is suspected with more than one lumbar spine surgery.

Natural History n

Progressive pain and in some cases disability

70

Diagnosis Differential diagnosis n Adjacent level disease n Arachnoiditis n Discitis n Inadequate decompression due to a sequestered free fragment, lateral disc herniation, or lateral recess stenosis n Inadequate fusion n Recurrent disc herniation n Spinal instability History n Need to inquire about the number and outcomes of previous surgeries n Differentiate structural problem versus a medical problem n Screen for the possibility of addiction disorders, somatization, and depression Exam Exam may be limited by severe pain. n Poor outcomes are predicted if patients have more than two out of five nonorganic findings as described by Waddell: – Tenderness in a superficial and nonanatomic distribution – Simulated axial loading or rotation – Distracted straight leg raise – Regional weakness or sensory disturbance – Overreaction n

Testing Laboratory tests include erythrocyte sedimentation rate and blood cultures in suspected disciitis. n Weight-bearing lateral flexion and extension films are used to rule out instability. n Pseudoarthosis is suggested if there is lucency around the pedicle screws or if there is a hardware failure. n MRI with contrast is useful in differentiating between scar tissue and a recurrent disc herniation or disciitis. n CT myelography is useful for documenting the bony involvement in lateral recess stenosis or central spinal stenosis. n Electrodiagnostic studies can be used to assess for peripheral neuropathy or nerve injury. n Selective nerve root blocks can be used to localize the level of the nerve root abnormality. n

Failed Back Surgery Syndrome

Discography can be used to identify a discogenic pain generator following posterior fusion.

Pitfalls Inability to identify underlying diagnosis following extensive assessment

n

Red Flags n n

Progressive neurologic dysfunction Bowel or bladder changes

Treatment Medical n Intensive multidisciplinary approach n NSAIDs n Muscle relaxants n Analgesics Exercises n General strengthening and stretching has been found to improve function and decrease use of pain medication. Modalities Heat, cold, ultrasound, and transcutaneous electrical nerve stimulation have been used for symptomatic relief of pain and muscle spasms.

n

Consults Physical medicine and rehabilitation n Neurologic or orthopedic-spine surgery n Pain management n Psychiatry or psychology n

Complications of treatment n Vascular injury or compartment syndrome n Initial hardware placement may stretch the nerve roots resulting in pain, which resolves over several weeks to months. n Hardware failure n Pain may also worsen following the completion of rehabilitation and returning to work

Prognosis n n n

n

Injection Trigger point injections for symptoms of myofascial pain n Zygapophyseal (facet) joint injection n Medial branch blocks/radiofrequency neurotomy n Epidural steroid injection for radicular symptoms n Discography n Spinal cord stimulation n Intrathecal pain medication n

Surgical n Revision surgery

Scar tissue due to arachnoiditis or epidural fibrosis does not respond to repeat surgery.

n

n

15% of surgical patients will develop disability and discomfort. Postoperative spondylolisthesis ranges from 10% to 12%. 5% to 15% of patients develop a recurrent disc herniation. One review reported success rates of >50% after the first surgery, 30% after the second surgery, 15% after the third surgery, and 5% after the fourth surgery. Up to 36% of patients develop adjacent level disease.

Helpful Hints n

Caution should be used in discouraging or detracting patients from appropriate diagnosis and treatment regardless of the poor outcomes with multiple spine surgeries.

Suggested Reading Hazard RG. Failed back surgery syndrome: surgical and nonsurgical approaches. Clin Orthop Relat Res. 2006;443:228–232.


n

71

Fractures, Lower Cervical Spine Description

n

Fractures of the lower cervical spine

Etiology/Types n

The Allen Ferguson scale is the most common classification system for subaxial cervical spinal injuries. – The scale is based on the mechanism of injury, which allows for prediction of bony and ligamentous injury. – It is categorized into six fracture types: compression–flexion, vertical compression, distraction flexion, compression extension, distraction extension, and lateral flexion.

Risk Factors n n

n n

Compression–flexion, distraction extension, and lateral flexion injuries each comprise about 20% of subaxial spine fractures. Vertical compression injuries make up 15%. Distraction flexion injuries make up 10%.

n

n

Pathogenesis Compression–flexion injuries are due to increased anterior column compression and posterior column distraction. – Subdivided from stage I representing a round and blunted anteriosuperior part of the vertebral body to stage V, >3 mm of retrolisthesis into the central canal, three-column spinal injury n Vertical compression injuries – Subdivided from stage I, central cupping fracture of the endplate, to stage III, posterior displacement of the vertebral body into the central canal n Distractive flexion injuries – Subdivided from stage I, blunting of the anteriosuperior vertebral body with 50%, angulation >20 degrees, lateral tilt >10 degrees, canal compromise >50 degrees, or posterior ligament disruption Flexion distraction injuries are treated surgically if there is ligamentous disruption.

At 2-year follow-up of thoracolumbar burst fractures, 49% had excellent pain and functional outcomes, 90% had satisfactory work status. 20-year follow-up of burst fractures without neurologic compromise, 88% of patients were able to work at their usual level of activity.

Helpful Hints n

Isolated L5 transverse process fracture is often associated with an underlying pelvic or sacral fracture.

n

Suggested Reading

Surgical Surgical fusion for complete dislocations, significant ligamentous, or soft tissue disruption, compression

Wood K, Buttermann G, Mehbod A, Garvey T, Jhanjee R, Sechriest V. Operative compared with nonoperative treatment of a thoracolumbar burst fracture without neurological deficit. A prospective, randomized study. J Bone Joint Surg Am. 2003;85-A(5):773–781.

n


Pitfalls Missed fractures n Overlooked spinal cord injury n

79

Giant Cell Tumor Description A giant cell tumor develops from non–bone-forming connective tissue and is the most common locally aggressive tumor with malignant potential.

Etiology/Types n n

Originate from the non–bone-forming connective tissue within the bone marrow Begins growing once skeletal maturity has occurred


Comprise 21% of all benign bone tumors and 5% of primary bone tumors Less than 10% become malignant Average age at diagnosis is 20 to 40 years Described in patients from 2 to 66 years of age Males are more likely to be diagnosed with a malignant tumor. Females are more likely to be diagnosed with a benign tumor.

Pathogenesis n

Unknown

Risk Factors n

Unknown


n

n

n

Most commonly found at the ends of long bones, such as the knee 8% to 12% of cases involve the axial spine In the axial spine, 68% occur in the sacrum, 11% occur in the cervical and lumbar spine, and 10% occur in the thoracic spine. Microscopically, contains a large number of osteoblast-like giant cells separated by mononuclear stromal cells. 88% of patients have neurologic dysfunction, which includes leg weakness or paresthesias, including perineal hypoesthesias, bowel and bladder dysfunction or paraplegia. Cervical spinal involvement includes dysphagia.

Natural History n

Progressive enlargement

80

Diagnosis Differential diagnosis n Aneurysmal bone cyst n Brown tumor of hyperparathyroidism n Chondroblastoma n Chondromyxoid fibroma n Enchondroma n Fibrous dysplasia n Simple bone cyst n Ossifying or nonossifying fibroma n Osteoblastoma n Osteosarcoma History Intermittent aching pain in the sacrum, lumbar, or cervical spine

n

Exam Axial spine or sacral tenderness n Localized swelling may be evident with superficial presentation. n Kyphosis and muscle spasm may also be noted in the cervical or lumbar region at the site of involvement. n Extracolonic mass on rectal examination with sacral presentations n Neurologic dysfunction n

Testing Laboratory tests may demonstrate anemia and an elevated erythrocyte sedimentation rate. – Serum calcium, phosphorus, and alkaline phosphatase tests can be used to differentiate the tumor from malignant giant cell tumor, hyperparathyroidism, and Paget’s disease. n X-rays may demonstrate an osteolytic lesion without surrounding reactive sclerosis or matrix mineralization. n CT can be used to define the extent of bony destruction. n MRI notes a low to intermediate signal on T1-weighted images and often low to high signal intensity on T2-weighted images. – Can be used to evaluate the extraosseous spread – Contrast enhancement varies n

Pitfalls Delay in diagnosis up to 3 years n Sacral presentations may be missed on routine X-rays. n

Giant Cell Tumor

n n

n

Neurologic deficits Unstable spine n

Treatment Medical n Staging is done with CT to determine bony involvement, MRI to assess the extraosseous spread Exercises n None

Prognosis n n n

Modalities None

n

Injection None

n

n

Surgical En bloc excision is the treatment of choice. n Radical excision is the treatment of choice followed by radiation, but surgery is often difficult or impossible. n Curettage has been shown to have a 50% recurrence rate in 5 years. n Embolization has been considered for presurgical treatment to decrease risk of profound bleeding or to eliminate the need for radiation. n

Radiation of giant cell tumors of the extremities is contraindicated due to the risk of malignant transformation The condition has been misdiagnosed as a radiculpathy or lumbar disc herniation and some even undergo discectomy.

n

Prognosis is based on complete tumor removal. Up to 50% of benign giant cell tumors recur. Complete or partial en bloc resection of the sacrum often includes the sacrifice of sacral nerve roots resulting in the loss of bowel, bladder, and sexual function. Mortality is associated with local invasion, malignant transformation, or renal failure due to neurogenic bladder. Mortality is 33% at 4 years following an extensive resection and reconstruction of a vertebral or sacral lesion.

Helpful Hints n n

44% recurrence rate for all giant cell tumors, with a 16.5% to 28% recurrence rate in the spine Neurologic deficits may be irreversible if there is a delay of more than 3 months before decompression

Consults Neurologic or orthopedic-spine surgery n Radiation oncology

Suggested Readings

Complications of treatment n Can be difficult to treat due to unpredictable behavior and location

Dahlin DC. Giant-cell tumor of vertebrae above the sacrum: a review of 31 cases. Cancer. 1977;39(3):1350–1356. Turcotte RE, Sim FH, Unni KK. Giant cell tumor of the sacrum. Clin Orthop Relat Res. 1993;(291):215–221.

n


Red Flags

81

Hemangiomas Description

n

Hemangiomas are benign vascular lesions in soft tissues or bones that are made up of cavernous, capillary, or venous blood vessels.

n n n n

Etiology/Types n

Unknown


Less than 1% of symptomatic primary bone tumors Prevalence increases with age and is most often identified by the fourth or fifth decade. Found in up to 12% of autopsies No gender preference

Pathogenesis n

Unknown

Risk Factors n

Increased intra-abdominal venous pressure during the third trimester of pregnancy may cause increased paravertebral venous plexus flow, causing a previously asymptomatic hemangioma to expand and bleed, resulting in associated neurologic deficits.

Gorham’s disease Metastasis Osler-Weber-Rendu disease Paget’s disease Skeletal lymphangiomatosis

History n Localized back or neck pain n Tenderness over the involved vertebral body n Associated muscle spasm n Neurologic dysfunction related to cord compression Exam Palpable swelling may be noted n Tenderness to palpation of the involved vertebral body n Associated muscle spasm n Kyphosis related to a thoracic compression fracture n Neurologic dysfunction n

Testing n X-rays demonstrate coarse vertical vertebral striations or a corduroy appearance of the vertebral body,

Clinical Features n

n

n n n n

Approximately 50% are found in the thoracic spine, followed by 39% in the lumbar spine and 7% in the cervical spine. Neurologic symptoms develop by enlargement of the vertebral body, leading to distortion or narrowing of the central canal, tumor extension into the epidural space, or compression fracture and associated bleeding into the epidural space. Multiple hemangiomas may cause spinal cord compression. Neurologic involvement is most common in the thoracic spine. May be related to pregnancy Rarely associated with spinal cord compression

Natural History n

Ranges from no progression over many years to progressive enlargement over months

Diagnosis Differential diagnosis Angiolipoma

n

82

Sagittal lumbar T2-weighted magnetic resonance image demonstrating increased signal within the vertebral bodies (arrows), compatible with a hemangioma. (Adapted from Fast A, Goldsher D. Navigating the Adult Spine: Bridging Clinical Practice and Neuroradiology. New York: Demos Medical Publishing, 2007:112.)

Hemangiomas

n

n n

Pitfalls n In 10% of cases with neurologic manifestations, pregnancy is a precipitating factor.

Red Flags n n

Progressive neurologic deficits Unstable spine

Surgical n Spinal cord compression requires surgical decompression with or without postoperative radiation. n Laminectomy can be associated with significant morbidity and mortality due to the potential of significant hemorrhage. n Angiography can be used for preoperative embolization to decrease the risk of hemorrhage. n Acute spinal cord injury requires surgical decompression. n Spinal instability may require fusion. Consults n Neurologic or orthopedic-spine surgery Complications of treatment n Hemorrhage with laminectomy n Delayed radiation-induced sarcoma

Prognosis n

Treatment Medical Symptoms may improve with unchanged radiographic appearance. n Hemangiomas respond to radiation treatment.

n

n

A 6-year follow-up of asymptomatic patients demonstrated no interval radiographic change of intraosseous lesions. A 9-year follow-up of patients describing localized pain thought to be related to the vertebral hemangioma did not have neurologic changes or imaging changes

Exercises n None

Helpful Hints

Modalities n None

Suggested Readings

Injection n Percutaneous vertebral augmentation can be used to strengthen the vertebral body if there is a risk of vertebral collapse and can provide symptomatic pain relief.

Acosta FL Jr, Sanai N, Chi JH, et al. Comprehensive management of symptomatic and aggressive vertebral hemangiomas. Neurosurg Clin N Am. 2008;19(1):17–29. Fox MW, Onofrio BM. The natural history and management of symptomatic and asymptomatic vertebral hemangiomas. J Neurosurg. 1993;78(1):36–45.

n

Management includes careful observation.


n

described as a “honeycomb” appearance; the vertebral body may be enlarged. Asymptomatic hemangiomas commonly appear on MRI in a portion of the lumbar vertebral body The increased T1 signal corresponds to the fatty stroma (relative proportion of adipocytes) and the increased T2 signal corresponds to the vasculature (vessels and interstitial edema). CT can demonstrate bony extension and possible involvement of the pedicle or neural arch. Bone scan demonstrates increased uptake at the site of the hemangioma.

83

Hemoglobinopathies (Sickle Cell Disease, Thalassemia) Description

n

Hemoglobinopathies describe a series of disorders that cause a defect in the production of hemoglobin.


Sickle cell anemia—hemoglobin SS ␤-thalassemia includes thalassemia major, intermedia trait, and a silent carrier. Other less common variants exist.

Epidemiology n

Sickle cell anemia is found in 1 of 625 Americans of African descent.

Thalassemia results in organomegaly, osteopenia, spinal cord compression due to extramedullary hematopoesis.

Natural History n

Variable

Diagnosis Differential diagnosis Abdominal disorders n Other causes of anemia n

History Acute low back pain with radiation and extremity pain n Abdominal pain n Muscle spasm n

Pathogenesis n n

n n

n

Adult hemoglobin (hemoglobin A) consists of two pairs of coiled α and ␤ chains. Hemoglobin S decreases solubility with deoxygenation, causing it to take on an irreversible “sickle” shape. Bone marrow hyperplasia and chronic anemia Thalassemia results from abnormal production of the α chain and its ␤, ␥, or ␦ chains, which causes early erythrocyte destruction. Tissue deoxygenation leads to bone marrow hyperplasia in the axial spine, increasing the risk of fractures.

Risk Factors n n

African, Asian, or Mediterranean descent Dehydration, infection, fever, or acidosis

Clinical Features n

Sickle cell disease – Acute low back with radiation and extremity pain are the most common complaint lasting about 4 to 5 days with no residual effects. – Abdominal pain – Bone infarction – Joint effusion or hemarthrosis – Septic arthritis – Osteomyelitis – Vertebral body compression fractures – Increased thoracic kyphosis and lumbar lordosis

84

Exam Febrile n Distress in acute sickling crises n Tenderness in the affected areas n Abdominal tenderness with normal bowel sounds n Thalassemia patients have altered skin pigmentation and hepatosplenomegaly. n Marrow hyperplasia in thalassemia patients causes bony expansion, resulting in frontal bossing and maxillary prominence. n

Testing Laboratory studies demonstrate anemia, leukocytosis, and mild thrombocytopenia with sickled cells and Howell-Jolly bodies. n Thalassemia results in a hypochromic, microcytic blood smear. n X-rays demonstrate cortical thinning and loss of bony trabeculae due to marrow hyperplasia. n Skull X-ray demonstrates a “hair-on-end” appearance. n Bone scan demonstrates increased uptake in areas of increased bone marrow. n MRI demonstrates replacement of fat by marrow. n

Pitfalls Differentiating bone infarction from osteomyelitis

n

Hemoglobinopathies n n

85

Bone marrow transplantation Lumbar bracing for vertebral body fractures or collapse

Exercises Sickle cell patients should exercise with caution due to an increased risk of acute sickle crisis. n Thalassemia patients have a diminished exercise capacity. n

Modalities Contraindicated in an acute crisis

n

Surgical n Surgical decompression of extramedullary marrow tissue compressing the spinal cord in thalassemia patients, followed by radiation treatment Sagittal lumbar T2-weighted magnetic resonance image demonstrating decreased signal throughout the vertebral bodies due to replacement of normal fatty stroma by hematopoietic cells in ␤-thalassemia.

Red Flags n n n n

Joint effusion or hemarthrosis Septic arthritis/osteomyelitis Pneumonia/pulmonary infarction Vertebral body compression fractures

Treatment Medical n Hydration n Analgesics, opioids n Hydroxyurea to increase fetal hemoglobin n Sulphasalazine n In thalassemia, blood transfusions suppress marrow hyperplasia resulting in bony pathology. Iron chelation is used to decrease iron overload; radiation to stop the overgrowth of extramedullary marrow.

Consults Hematology n Neurological or orthopedic-spine surgery n

Complications of treatment n Multiple blood transfusions in thalassemia patients increase the risk of infectious disease, iron overload, and formation of antibodies. n Surgical risk due to low platelet count, poor bone mass, anemia, or cardiomyopathy

Prognosis n

Sickle cell patients and thalassemia patients may live up to the fourth decade.

Helpful Hints n

Patients may appear comfortable but report excruciating pain.

Suggested Reading Cordner S, De Ceulaer K. Musculoskeletal manifestations of hemoglobinopathies. Curr Opin Rheumatol. 2003;15(1):44–47.


Injection n None

Hyperparathyroidism Description

Natural History

Hyperparathyroidism causes the increased secretion of parathyroid hormone (PTH) resulting in bone loss and spinal deformity from fractures of the vertebral body.

n

Vertebral fractures due to progressive kyphosis with associated constitutional symptoms such as abdominal pain, renal failure, hypertension, mental status changes, and coma

Etiology/Types n

n

Primary hyperparathyroidism is a result of abnormal growth of the parathyroid glands due to an adenoma, multiple adenomas, carcinoma, or diffuse hyperplasia. Secondary hyperparathyroidism is the increased secretion of PTH in response to low serum calcium caused by kidney dysfunction or decreased vitamin D metabolism.

Diagnosis Differential diagnosis Hypophosphatemia n Neoplasms n Sarcoidosis n

History Deep bony pain n Muscle and joint pain n Weakness and fatigue n Nausea and vomiting n

Epidemiology n n n

Unknown prevalence Male to female ratio is 1:3 Hyperparathyroidism is associated with multiple endocrine neoplasia type I and IIa syndromes.

Pathogenesis n

n

PTH is responsible for maintaining serum calcium levels by synthesizing the active form of vitamin D, stimulating intestinal and renal uptake of calcium, activating osteoclastic bony resorption, and increasing phosphate excretion. Persistently elevated PTH causes bony demineralization.

Risk Factors n

Multiple endocrine neoplasms type I and IIa

Clinical Features n n n n n n n n n n

Bone pain or vertebral body compression fracture 20% report generalized myalgias and arthralgias. 10% to 20% of patients also develop nephrolithiasis. 25% of patients are at risk for osteopenia and vertebral fractures. 50% of patients with slight serum calcium elevations may report weakness and fatigue. 20% describe gastrointestinal symptoms such as nausea, vomiting, constipation, anorexia, abdominal pain. 3.8% of patients also present with pseudogout. Other neurologic changes include changes in mental status and coma. Renal failure Hypertension

86

Exam Vertebral body compression fractures may be noted with tenderness to palpation of the involved bony segment with associated local muscle spasm.

n

Testing 96% of primary hyperparathyroidism patients demonstrate increased serum calcium levels. n Low serum phosphorus n Elevated serum alkaline phosphatase and chloride n Elevated urinary calcium secretion n Secondary hyperparathyroidism demonstrates elevated serum phosphorus levels and rarely demonstrates increased serum calcium levels. n PTH assay n Bone biopsy, which is rarely done, demonstrates increased osteoclasts. n Electrocardiogram may demonstrate a shortened QT interval n X-rays demonstrate subperiosteal bone resorption on the radial aspects of the middle phalanges, resorption of the terminal tufts of the phalanges, cystic lesions in the long bones, and a “salt and pepper” appearance in the skull. n Resorption may occur at the pubic symphysis along with sclerosis of the sacroiliac joints, which may result in sacroiliac joint instability. n Anterior wedging and osteopenia of the vertebral bodies n Secondary hyperparathyroidism results in arterial calcification and osteosclerosis of soft tissues. n

Hyperparathyroidism

n n

Bone scan is used to identify affected parathyroid tissue. SPECT may be used to detect a parathyroid adenoma. Enlarged glands can be identified with CT or ultrasound.

Pitfalls n Overlooked diagnosis

Red Flags n

Changes in mental status, coma, muscle weakness, hypotonia, fatigue, anorexia, renal failure, hypertension

Treatment Medical n No effective medical treatment for primary hyperparathyroidism. n NSAIDs or analgesics for vertebral body compression fractures. Exercises n General strengthening and stretching Modalities n Heat, cold, ultrasound, and transcutaneous electrical nerve stimulation have been used for symptomatic relief of pain and muscle spasms. Injection Percutaneous vertebral augmentation for treatment of compression fractures

n

Surgical n Surgical resection of affected parathyroid tissue is the most definitive treatment. n Postoperative therapy may include calcium and vitamin D, phosphorus, and magnesium. n Treatment of secondary hyperparathyroidism requires control of the underlying disease. Consults Endocrinology n Otolaryngology n


Prognosis n n

n n

Patients who are asymptomatic with mildly elevated serum calcium may be followed. Patients who become symptomatic require surgical removal and occasionally may require a reoperation. Bony lesions heal once the source of excess PTH is removed. Large cysts may not heal and may result in pathologic fractures.

Helpful Hints n

Important to screen for possible underlying etiology

Suggested Reading Petti GH Jr. Hyperparathyroidism. Otolaryngol Clin North Am. 1990;23(2):339–355.


n

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Low Back Strain Description

n

A low back strain results from an injury to the dynamic muscle stabilizers or static ligamentous structures of the lower back.

n

Etiology/Types n

May be associated with mechanical overload or a prolonged abnormal posture

Epidemiology n

Represents 60% to 70% of all mechanical low back pain presentations


May be related to ligamentous or muscular injury from excessive tension or stretching Muscle fatigue from overuse Muscle spasm caused by muscle overload Paraspinal muscle deconditioning due to previous injury

Risk Factors n n n

Mechanical overload Muscle overuse Prolonged abnormal posture


Localized or diffuse nonradiating lower back pain Worsened with abnormal or static posture

n

Exam Normal neurologic examination n Tenderness to palpation of paraspinal muscles, most often at the L5–S1 region n Decreased lumbar range of motion n Supraspinatus ligamentous strains are tender with palpation. n

Testing X-rays are usually normal. n MRI or CT studies often do not clarify the diagnosis. n Asymptomatic congenital findings such as spina bifida occulta, lumbarization of the S1, or sacralization of the L5 occur in about 5% of the population. n

Pitfalls Lack of correlation of the history to the physical examination

n

Red Flags n n n

Natural History n

Usually a self-limiting condition that may last 6 to 12 weeks

Diagnosis Differential diagnosis n Herniated nucleus pulposus n Osteoarthritis n Posterior element or vertebral body fractures n Scoliosis n Soft tissue or bony trauma n Spondyloarthropathies n Tumors History Dull, aching pain n Localized or diffuse lower back pain n

88

Possible radiation into the buttocks but not into the lower extremities Pain with flexion and/or extension Worsened with activity or static postures and improved with recumbency

n

Neurologic changes Soft tissue or bony abnormalities Skin rashes Severe pain

Treatment Medical NSAIDs n Muscle relaxants n Opioids if the pain is deemed severe n Limited use of a lumbar corset n Acupuncture has been described as helpful for symptomatic relief. n

Exercises Minimal or no bed rest n Physical activity within the patient’s pain tolerance n Physical therapy and a home exercise program focused on pain control and regaining mobility n

Low Back Strain

Injection Trigger point injections to block the reflexive spasm, if 2 to 4 weeks have passed without significant improvement

n

Surgical None

n

Consults n Physical medicine and rehabilitation Complications of treatment Persistent pain for months or years n Recurrent episodes of increasing frequency and intensity n

Prognosis n n

Up to 90% of cases resolve within 2 months. Within 3 to 5 years, there is up to a 60% chance of recurrence.

Helpful Hints n n

Generally thought to be a self-limiting condition The physician should reassure the patient that no damage will occur with continued activity.

Suggested Readings Deyo RA, Weinstein JN. Low back pain. N Engl J Med. 2001;344(5):363–370. Panagos A, Sable AW, Zuhosky JP, Irwin RW, Sullivan WJ, Foye PM. Industrial medicine and acute musculoskeletal rehabilitation. 1. Diagnostic testing in industrial and acute musculoskeletal injuries. Arch Phys Med Rehabil. 2007;88 (3 Suppl 1):S3–S9.



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Lymphoma Description

n

Lymphoma is a malignant disease of lymphoreticular origin that usually arises from the lymph nodes.

Diagnosis

Etiology/Types Hodgkin’s lymphoma Non-Hodgkin’s lymphoma – B cell lymphoma (most common) – T cell lymphoma – Natural killer (NK) cell lymphoma – Immunodeficiency-associated lymphoproliferative disorders n Staging (stages I to IV) and grading from low to high for non-Hodgkin’s lymphoma allow for further classification n Unknown etiology n n


The annual incidence is 40 to 60 cases per million individuals. Bony involvement is due to hematogenous spread or direct extension by the tumor. Most commonly occurs between 20 and 60 years of age. Male to female ratio of 2:1 The lumbosacral spine is involved in 55% of cases, the thoracic spine 34% of cases, and the cervical spine 11% of cases.

Pathogenesis n n

Generally unknown Extraosseous lesions may be related to osteoclastic cytokines produced by the malignant cells.


Autoimmune disease Epstein-Barr virus infection HIV or HTLV-1 infection Increasing age Positive family history


Persistent pain over the affected bony region Most often invades the axial spine

Natural History n

Remission is possible in certain types of lymphomas if the disease is not too extensive.

90

5-year survival rate approaches 50%.

Differential diagnosis Eosinophilic granuloma n Neoplasm of the breast or prostate n Paget’s disease n

History Persistent pain over the affected bony area n Pain is worsened with recumbent position. n Increased bony pain with the consumption of alcohol n Multiple lesions may result in constitutional symptoms such as fever. n Neurologic manifestations with invasion of the peripheral nerves or the central spinal canal n

Exam Bony tenderness to palpation and a soft tissue mass of the affected bone n Characteristic tenderness over a pathologic compression fracture n Neurologic deficits n Lymphadenopathy and splenomegaly in patients with generalized disease n

Testing Laboratory studies are usually normal, although anemia with an increased erythrocyte sedimentation rate and increased serum proteins may indicate extension into other tissues. n Histologic findings include Reed-Steinberg cells, atypical mononuclear cells n X-rays may demonstrate lytic, sclerotic, periosteal lesions, or a compression fracture n Primarily invades the vertebral body followed by the posterior elements. n Bone scan may be used to detect multiple lesions and for monitoring the response to chemotherapy. n CT is used for staging purposes and to assess bony involvement. n MRI may detect early changes in bone and lymph node involvement. n Positron emission tomography (PET) scan n Bone marrow aspiration n

Pitfalls Inadequate staging

n

Lymphoma

Acute onset of paraparesis or cauda equina syndrome with epidural lymphomas

Treatment Medical Radiation therapy and/or chemotherapy based on staging n Rituximab (anti-CD-20 monoclonal antibodies) n Stem cell transplant n

Exercises n None

Consults n Hematology oncology n Radiation oncology n Neurologic or orthopedic-spine surgery Complications of treatment n Complications related to chemotherapeutic agents, surgery, and radiation

Prognosis n n

Significant deficits in mobility may be possible with epidural disease The 5-year survival rate is 50%.

Helpful Hints Plain radiographs are an easy tool to use to evaluate for the localized bony manifestations of lymphoma.

Modalities n None

n

Injection None

Suggested Readings

n

Surgical Surgical decompression is considered in younger patients with rapidly progressive paralysis.

n

Eichler AF, Batchelor TT. Primary central nervous system lymphoma: presentation, diagnosis and staging. Neurosurg Focus. 2006;21(5):E15. Citow JS, Rini B, Wollmann R, Macdonald RL. Isolated, primary extranodal Hodgkin’s disease of the spine: case report. Neurosurgery. 2001;49(2):453–456.


Red Flags n

91

Marfan Syndrome Description

Natural History

Marfan syndrome is a connective tissue disorder that primarily affects the skeletal, cardiovascular, and ocular systems.

n

Etiology/Types n

Caused by a defect of the fibrillin protein, which is a component of connective tissue microfibrils.

Epidemiology n n n

Occurs in 1 in 10,000 individuals. 15% of patients are the result of a spontaneous mutation. No gender preference

Pathogenesis n n n

Autosomal dominant Defect of the fibrillin-1 gene on chromosome 15 (FBN1) Defect in fibrillin synthesis, secretion, and matrix formation

Risk Factors n

Genetic predisposition

Clinical Features n n n n n n n n

n n n n

Tall and thin stature Long arms compared to the trunk Joint laxity Loss of thoracic kyphosis Multilevel scoliosis occurs in 62% of patients. Restrictive lung disease due to scoliosis Pectus excavatum (chest depression) and pectus carinatum (pigeon chest) occur in 66% of patients. Dural ectasia or a ballooning of the dural sac, may be asymptomatic or result in back pain and headaches Atlantoaxial subluxation Cervical spinal stenosis Arachnodactyly 1996 diagnostic criteria include major [4 of 8 skeletal manifestations (see Suggested Readings), lumbosacral dural ectasis, aortic dilatation, and ectopia lentic], and minor criteria (joint hypermobility, myopia, recurrent hernia, mitral valve prolapse).

92

Unknown

Diagnosis Differential diagnosis Ehlers-Danlos syndrome n Osteogenesis imperfecta n

History Back pain and headaches may be due to dural ectasia.

n

Exam Tall thin stature n Neurologic deficits may be due to dural ectasia. n Pectus excavatum n Pectus carinatum n Joint laxity n

Testing Plain radiographs demonstrate thoracolumbar scoliosis, increased vertebral body height, and posterior scalloping of the vertebral bodies. n MRI can be useful for assessing possible dural ectasia and cervical spinal stenosis. n Plain radiographs or CT can be used to assess atlantoaxial subluxation. n

Pitfalls n Dural ectasia

Red Flags n n n n

Aortic dissection Retinal detachment Severe mitral valve regurgitation Severe pectus excavatum resulting in cardiopulmonary compromise

Treatment Medical Bracing to prevent progressive scoliosis found to only be successful in 17% of patients. n Bracing recommended for curves up to 25 degrees and not suggested for curves greater than 40 degrees n Bracing may begin early in life. n

Exercises General strengthening n Stabilization exercises n

Marfan Syndrome

Caution with cardiovascular conditioning


Prognosis n n n

Continued progressive neurologic decline without treatment Average life expectancy is 70 years of age. Disease manifestations in the axial spine are unknown

Injection Trigger point injections and epidural steroid injections have been used for symptomatic relief.

Helpful Hints

Surgical n Surgical deformity correction is considered with scoliotic curves >40 degrees.

Suggested Readings

n

Consults Physical medicine and rehabilitation n Neurologic or orthopedic-spine surgery n Rheumatology n


n

Be aware of the risk of aortic dissection and dural ectasia that may be the source of axial spine pain.

Demetracopoulos CA, Sponseller PD. Spinal deformities in Marfan syndrome. Orthop Clin North Am. 2007;38(4):563–572. De Paepe A, Devereux RB, Dietz HC, Hennekam RC, Pyeritz RE. Revised diagnostic criteria for the Marfan syndrome. Am J Med Genet. 1996;62(4):417–426. Giampietro PF, Raggio C, Davis JG. Marfan syndrome: orthopedic and genetic review. Curr Opin Pediatr. 2002;14(1):35–41. Sponseller PD, Bhimani M, Solacoff D, Dormans JP. Results of brace treatment of scoliosis in Marfan syndrome. Spine. 2000;25(18):2350–2354.


n

93

Meningioma Description Meningioma is a benign tumor that makes up 25% to 45% of all intradural spinal neoplasms.

Etiology/Types n

Generally unknown, but thought to originate from arachnoidal cells.


Spinal meningiomas make up about 12% of all meningiomas. The annual incidence is thought to be 0.5 to 2 per 100,000 individuals. Typically affects patients older than 50 years of age 80% of patients are female.

Pathogenesis n n n

Slow growing tumor Remains intradural Most common in the thoracic spine with occasional appearance in the cervical and lumbosacral spine

History Midline axial or radicular back pain is the most common complaint. n Neurologic complaints include weakness, numbness, and paresthesias. n

Exam n The most common initial findings are sensory changes, gait ataxia, and weakness. n Ranges from nonspecific low back paraspinal tenderness to neurologic findings of myelopathy Testing X-rays may pick up the intradural tumor if it contains calcium n MRI with contrast is the best imaging study to identify the tumor location and its relation to the surrounding tissues. n

Pitfalls n Delay in diagnosis may be up to 2 years

Risk Factors n

Unknown

Clinical Features n

The most common complaint is back pain, although other signs include weakness, numbness, parasthesias, and gait ataxia.

Natural History n

Slow-growing tumor that is first noted with progressive neurologic findings

Diagnosis Differential diagnosis Abscess n Chordoma n Fibroma n Lipoma n Lymphoma n Metastasis n Vascular malformation n

94

Axial thoracic T1-weighted magnetic resonance image demonstrating a large meningioma within the spinal canal (arrows). (Adapted from Fast A, Goldsher D. Navigating the Adult Spine: Bridging Clinical Practice and Neuroradiology. New York: Demos Medical Publishing, 2007:114.)

Meningioma

Red Flags n

Spinal cord compression or myelopathy

Treatment Medical Radiation therapy n Chemotherapy n

Exercises None

n

Modalities None

n

95

Neurologic or orthopedic-spine surgery


Prognosis n n n n

13% of patients can have severe functional deficits. Mean survival of a low-grade meningioma is 20 years. Mean survival of a high-grade meningioma is 12 months. Recurrence rate of 10%

n

Surgical The treatment of choice is excision of the tumor and its dural attachment.

Helpful Hints n

Progressive neurologic decline may lead to permanent functional deficits.

n

Suggested Readings

Consults Hematology oncology n Radiation oncology

Barnholtz-Sloan JS, Kruchko C. Meningiomas: causes and risk factors. Neurosurg Focus. 2007;23(4):E2. Setzer M, Vatter H, Marquardt G, Seifert V, Vrionis FD. Management of spinal meningiomas: surgical results and a review of the literature. Neurosurg Focus. 2007;23(4):E14.

n


Injection n None

Meningitis Description

Clinical Features

Meningitis is an infection of the meningeal lining of the central nervous system.

n

Etiology/Types n

n n n n

The most common bacteria are Streptococcus pneumoniae, Haemophilus influenzae, and Neisseria meningitides. Staphylococcus aureus is associated with neurosurgical procedures. Staphylococcus epidermidis is associated with ventriculoperitoneal shunts. Most common viral causes are coxsackievirus, echovirus, and retrovirus. Also caused by fungi, mycobacteria, protozoa, and spirochetes

Epidemiology n

n

n

n

Annual incidence of bacterial meningitis is 5 cases per 100,000 adults per year in developed countries. 80% of cases of adult bacterial meningitis are caused by Streptococcus pneumoniae and Neisseria meningitides. Childhood meningitis is most commonly caused by Haemophilus influenzae B, Streptococcus, and Escherichia coli. Annual incidence of viral meningitis is thought to be 7.6 cases per 100,000 adults per year.

Pathogenesis n

n

n n

Results in the spread of polymorphonuclear leukocyte exudate in the subarachnoid space throughout the meninges covering the brain and spinal cord. Lower levels of immune cells in the subarachnoid space compared with serum concentrations allowing the organism to spread more rapidly Thickened fluid slows the flow of CSF, resulting in mental status changes. Meningitis of fungal, tuberculous, protozoan, and spirochetal origin result in slow gradual changes in mental status.

Risk Factors n n

Immunocompromised state Young adults

96

Classic symptoms of neck stiffness, fever, and altered mental status occur in 44% of patients; 95% of these demonstrate two of the three symptoms n In patients with bacterial meningitis: – 87% complain of headache – 83% complain of neck stiffness – 77% complain of fever – 69% had a change in cognition, nausea, vomiting, and photophobia n Bacterial meningitis mental status changes can occur as quickly as 24 to 36 hours. n Headache is the most common symptom of fungal meningitis.

Natural History n

Progressive mental status changes associated with neck stiffness leading to death.

Diagnosis Differential diagnosis Aseptic meningitis due to inflammatory diseases n Brain abscess n Epidural abscess n Posterior fossa tumor n Spontaneous cerebrospinal fluid leak n Subarachnoid hemorrhage n Subdural empyema in patients with mastoiditis or sinusitis n

History Classic triad features include neck stiffness, fever, and altered mental status.

n

Exam Changes in mental status; coma n Febrile n Nuchal rigidity or neck stiffness is assessed by forward flexion of the neck while the patient is in a supine position (30% sensitivity, 68% specificity). n Brudzinski’s sign is positive: hip and knee flexion occur during passive neck flexion. n Kerning’s sign is positive: when the patient is in a supine position, the thigh is flexed toward the abdomen, and the patient resists knee extension. n

Meningitis

Pitfalls Aggressive diagnosis and treatment can lead to full recovery. n Delay in diagnosis and treatment significantly increases morbidity and mortality. n

Exercises n None Modalities n None Injection n None Surgical n None Consults n Infectious disease Complications of treatment n Cerebral edema/infarction n Seizures n Hydrocephalus n Hypotension n Septic shock n Acute respiratory distress syndrome

Prognosis n

Red Flags n

CT may be done prior to a lumbar puncture, as a sudden decrease of intracranial pressure may result in acute compression of the brainstem.

n n n

Treatment Medical n Due to the high potential mortality, empiric treatment and diagnostic workup should occur simultaneously. n Intravenous antibiotics include vancomycin, penicillin, ampicillin, ceftriaxone. n Aseptic meningitis is treated symptomatically.

Aggressive diagnosis and treatment can lead to full recovery. Delay in diagnosis and treatment significantly increases morbidity and mortality. Aseptic meningitis resolves within several weeks. Mortality rate up to 25%

Helpful Hints n

Due to the high potential mortality, empiric treatment and the diagnostic workup should occur simultaneously.

Suggested Reading Schut ES, de Gans J, van de Beek D. Community-acquired bacterial meningitis in adults. Pract Neurol. 2008;8(1):8–23.


Testing Laboratory testing can demonstrate increased white blood cells, an increased erythrocyte sedimentation rate, and C-reactive protein. n Lumbar spinal tap with cerebrospinal fluid culture n Bacterial meningitis results in a turbid fluid, >1,000 white blood cells/mm3, polymorphonuclear leukocytes, decreased glucose, protein level >100 mg/dl and gram-positive organisms. n Viral meningitis results in 6 months.

n

Red Flags n

Signs and symptoms consistent with spinal cord compression or cauda equine syndrome

Treatment

Modalities n None Injection n None Surgical n Decompressive surgery with fusion for spinal instability Consults Neurologic and orthopedic-spine surgery n Radiation oncology n Hematology oncology n Physical medicine and rehabilitation n

Complications of treatment n Spinal cord compression or cauda equina syndrome with delayed decompression

Prognosis n

Mean survival is 3 to 5 years

Medical Chemotherapy n Radiation therapy n Bone marrow transplantation

Helpful Hints

Exercises n Patient education n Strengthening of the muscles surrounding the long bones n Cardiovascular conditioning as tolerated

Suggested Readings

n

n

Emergent surgical decompression for progressive spinal cord compression or cauda equina syndrome

Bilsky MH, Azeem S. Multiple myeloma: primary bone tumor with systemic manifestations. Neurosurg Clin N Am. 2008;19(1):31–40. Esteve FR, Roodman GD. Pathophysiology of myeloma bone disease. Best Pract Res Clin Haematol. 2007;20(4):613–624.


n

thrombocytopenia, a positive Coombs test, elevated erythrocyte sedimentation rate, hypercalcemia, hyperuricemia, increased creatinine. Impaired coagulation cascade Increased total serum protein concentrations including increased M proteins Bence-Jones proteinuria X-rays demonstrate characteristic osteolysis of the vertebral bodies with posterior element sparing CT demonstrates vertebral body involvement and the extent of bony destruction. MRI demonstrates changes in bone marrow.

99

Multiple Sclerosis Description

n

Multiple sclerosis is a chronic inflammatory disease affecting the central nervous system that varies in its progression and may lead to significant morbidity, including deficits in cognition, mobility, and activities of daily living.

n n n n n n


n n n

Thought to be related to a viral or autoimmune mechanism Genetic predisposition Relapsing–remitting type (most common): relapses with partial or complete remissions without significant progressive deterioration. Primary progressive: primary deterioration with no relapses or remission Secondary progressive: progressive deterioration with relapsing remitting episodes Progressive: relapsing type


Prevalence ranges from 40 to 220 per 100,000 in the United States. Prevalence increases in higher latitudes. Spinal cord involvement occurs in 9% to 25% of patients. Primary spinal cord involvement occurs in 2% to 10% of patients. Younger patients tend to follow a relapsing–remitting course, whereas older individuals follow a primary progressive course.

Pathogenesis n n n

Multifocal demyelinated plaques are scattered throughout the central nervous system. Disease results in demyelization and axonal damage. Affects the gray and white matter

Risk Factors n n

Genetic predisposition Higher geographic latitudes

Clinical Features n

n

Clinical diagnosis is based on two or more neurologic episodes in two or more areas of the central nervous system. Unilateral optic neuritis

100

n n n

Diplopia Optic neuritis Sensory dysfunction Gait ataxia Spasticity Pain Neurogenic bowel or bladder dysfunction Fatigue Temperature sensitivity Cognitive changes

Natural History n

The disease process begins long before the development of symptoms.

Diagnosis Differential diagnosis Devic disease n Infection n Neoplasm n Spinal cord infarct n Transverse myelitis n

History Motor or sensory dysfunction n Fatigue n Temperature sensitivity n Problems with balance and gait n

Exam Positive Lhermitte’s sign n Motor deficits n Gait ataxia n Neurogenic bowel or bladder dysfunction n Disability is measured using Kurtzke’s expanded disability status scale ranging from 0.0 (normal) to 10.0 (death). n

Testing n Laboratory testing demonstrates oligoclonal bands or IgG within the CSF. n MRI is used for diagnosis and demonstrates “plaquelike” lesions of increased signal on T2-weighted images within the spinal cord or brain. – Preference for dorsolateral aspect of the spinal cord n Dawson’s fingers are the characteristic lesions surrounding the deep veins of the brain.

Multiple Sclerosis n

101

Avoidance of increased environmental temperatures, which results in increased fatigue and weakness

Exercises General strengthening at a moderate intensity in colder temperatures n Endurance training at a low or moderate intensity n Pool therapy n Stretching Modalities n Heat, cold, ultrasound, and transcutaneous electrical nerve stimulation have been used for symptomatic relief of local pain and muscle spasms. Injection None

n

Surgical n None Sagittal cervical T2-weighted magnetic resonance image demonstrating minimal increased signal within the spinal cord at the C4–C5 level (arrow) resulting from multiple sclerosis.

n n n

48% of patients have positive findings in the cervical spinal cord. Visual and auditory evoked potentials Somatosensory evoked potentials

Pitfalls n Delay in diagnosis

Consults n Neurology Complications of treatment n Patients may develop neutralizing antibodies to the medications within 2 years, decreasing their effectiveness. If no antibodies develop there is no concern about antibody development thereafter.

Prognosis n n

Red Flags n n

Progressive neurologic decline Bowel or bladder dysfunction

Treatment Medical n Intravenous (IV) methylprednisolone 1,000 mg for 3 days, which helps to speed recovery during an acute exacerbation n Disease-modifying drugs have been shown to be effective, primarily against the relapsing–remitting type. n Interferon ␤-1b, interferon ␤-1a, glatiramer acetate, mitoxantrone n Symptomatic treatment is directed at neurogenic bladder, fatigue, heat intolerance, spasms, pain, cognition and mood, speech, and swallowing.

n n n n

Variable Spinal cord plaques found on MRI correlate with the degree of disability. Median time from symptoms onset until use of a cane is 20 years. Median time from symptoms onset until use of a wheelchair is 30 years. 50% of patients will need assistance ambulating within 15 years after onset. Unknown how well the medications reduce disability

Helpful Hints n

Global assessment is important due to the diffuse involvement of the central nervous system.

Suggested Reading Noseworthy JH, Lucchinetti C, Rodriguez M, Weinshenker BG. Multiple sclerosis. N Engl J Med. 2000;343(13):938–952.


n

Myofascial Pain Syndrome Description

n

Myofascial pain syndrome is a regional pain disorder characterized by a localized hyperirritable and hypersensitive palpable area within a taut band of skeletal muscle or muscle fascia that refers pain in a distal nondermatomal distribution when compressed.

n n n

Clinical Features n

Etiology/Types n

Unknown

Epidemiology n n

n

Occurs in 30% of patients in a general medical clinic and up to 93% of patients referred to a pain clinic Latent trigger points are trigger points that are tender to palpation, which may be associated with stiffness and decreased range of motion that is not associated with complaints of pain. Active trigger points are trigger points associated with pain complaints.

Pathogenesis n

n

n

n

Myofascial trigger points produce motor changes, sensory hyperalgesia and dysesthesias, and autonomic symptoms that include salivation, changes in skin temperature, sweating, and proprioceptive changes. The local twitch response is a brisk contraction of muscle fibers in a taut band that is elicited by snapping palpation or the insertion of a needle that is thought to correlate with an increased density of sensory receptors and spontaneous electrical activity close to motor endplates. Sustained release of acetylcholine at the motor end plates with sustained muscle contraction and local ischemia results in the release of inflammatory substances causing muscle pain. Spinal segmental sensitization may develop if myofascial pain is left untreated.


Anxiety Chronic infection Chronic muscle imbalance Degenerative joint disease Nerve root compression or irritation Nutritional deficiencies Poor posture or ergonomics Repetitive strain injuries or repetitive microtrauma

102

Scoliosis Sleep deprivation Thyroid disorders Traumatic injury

n n n n n

Sudden onset Pain in a distributed pattern Restricted joint range of motion with increased sensitivity to stretching Muscle weakness due to pain with no muscular atrophy Palpation of the painful site resulting in a reproduction of the characteristic pain A palpable muscle band with a local twitch response

Natural History n

General worsening of pain complaints

Diagnosis Differential diagnosis Chronic pain syndrome n Fibromyalgia n Fracture n Infection n Joint osteoarthritis n Neoplasm n Psychological disorders n Polymyalgia rheumatica n Polymyositis n Radiculopathy n

History Localized or regional deep aching pain n Pain intensity ranges from mild to severe. n Stiff joints n Fatigue/weakness n Sleep difficulty n Parasthesias n Numbness n

Exam Posture asymmetry n Active and passive range of motion restrictions n Abnormal movement patterns n Palpation of trigger point n The trigger point often has a “ropelike” consistency n

Myofascial Pain Syndrome

Pitfalls Often underdiagnosed and undertreated n Unemployment, poor coping ability, and constant pain are related to poor treatment. n

Red Flags n n n n

Fracture Neoplasm Neurologic deficits Infection

Treatment Medical n Acetaminophen n Muscle relaxants n NSAIDs n Analgesics n Dry needling Exercises n The use of vapocoolant spray over the entire trigger point region and reference zone followed by passive muscle stretching n Progressive stretching and strengthening Modalities n Heat, cold, ultrasound, and transcutaneous electrical nerve stimulation have been used for symptomatic relief of pain and muscle spasms. n Massage

n

Ischemic compression

Injection n Trigger point injections with the trigger point stabilized between the thumb and forefinger using local anesthetic [procaine (higher risk of anaphylaxis) or lidocaine], which decreases local soreness n A local twitch response is critical for immediate relief of muscle tightness and pain. n Corticosteroids, saline, and botulinum toxin have also been used in injections. n Paraspinous block with local anesthetic Surgical n None Consults n None Complications of treatment n Trigger point injections have a low risk of complications, which include bleeding, infection, allergic reaction to the injected medications.

Prognosis n

Few studies have been completed that demonstrate patients are able to increase their coping skills and life satisfaction while decreasing sick time.

Helpful Hints n

Generally underdiagnosed and undertreated

Suggested Reading Borg-Stein J, Simons DG. Focused review: myofascial pain. Arch Phys Med Rehabil. 2002;83(3 Suppl 1):S40–S47, S48–S49.


Testing n Algometry as described by Fischer n Imaging can be used to rule out other conditions.

103

Neck Pain Associated with Occupation Description

n

Acute or chronic neck pain associated with occupational activities. Also known as repetitive strain injury (RSI), cumulative trauma disorder (CTD), occupational cervicobrachial disorder (OCD), and work-related musculoskeletal disorder (WMSD).

n n n

Clinical Features n

Etiology/Types n

Neck pain probably arises from a combination of individual and workplace factors.


Prevalence of neck pain in workers ranges from 27% to 49%. 11% to 14% of workers annually are limited in activities due to neck pain. The highest prevalence of occupational neck pain is found in office and hospital workers. The lowest prevalence of occupational neck pain is found in forest and industrial workers.

Pathogenesis n n

n

n

n

Excess shoulder girdle muscles loading Muscle strains are considered unlikely with computer use as there is less than 5% of maximal voluntary contraction. Increased cervical pain is associated with decreased cervical rotation and increased activity in the superficial cervical flexors with an associated compensatory decreased activity in the deep cervical flexors. Muscle biopsy results note increased fiber crosssectional areas and mitochondrial disturbances of type 1 fibers. Increased inflammatory mediators have been found in local muscles that correlate with pain.


Female gender Forceful exertions High job demands High level static contractions Increasing age, particularly in the fourth and fifth decade of life Low physical capacity Previous musculoskeletal pain Poor social support at work Poor work posture

104

Poor workstation ergonomics Prolonged static loads and extreme postures Repetitive job tasks Sedentary job activities

Neck pain without symptoms in the lower extremities

Natural History n

Variable

Diagnosis Differential diagnosis Infection n Osteoarthritis n Radiculopathy n Referred pain from cardiothoracic structures n Tumor n

History Increased pain, tiredness, and stiffness n Pain worse during workday and improved during weekend n Sleep difficulty n Associated headaches n

Exam Poor posture/head forward posture n Decreased cervical range of motion, particularly with rotation n Increased muscle tension in the upper trapezii, levator scapulae, and scalenes n Tenderness to palpation of the superior nuchal line n

Testing Plain radiographs may demonstrate loss of the normal lordotic curve suggesting spasm. n Magnetic resonance imaging may be used to rule out soft tissue pathology. n Electrodiagnostic studies can be used to assess for radiculopathy. n

Pitfalls Overlooking workplace and psychological factors

n

Red Flags n

Weakness, numbness, or tingling

Neck Pain Associated with Occupation

Acute pain and muscle spasm that may be associated with a fracture.

Treatment Medical Cognitive behavioral therapy n Ergonomic interventions have not been shown to prevent neck pain in the literature, although a thorough discussion may uncover poor workstation ergonomics that can be easily altered. n Analgesics n NSAIDs n Acupuncture has been described to be helpful for symptomatic relief. n

Exercises Exercise program focusing on motor relearning training n Manipulation n Mobilization n

Surgical n Surgical decompression for radicular symptoms can produce rapid and significant symptom relief. n Percutaneous or open surgical treatment of neck pain without radicular symptoms lacks evidence. Consults Psychology or psychiatry n Physical medicine and rehabilitation n Neurologic or orthopedic-spine surgery for surgical indications n

Complications of treatment Less than 1% of cervical epidural steroid injections result in serious adverse reactions. n 4% of open surgical procedures in the cervical spine can result in serious adverse reactions. n

Prognosis n n

Modalities n Heat, cold, ultrasound, and transcutaneous electrical nerve stimulation have been used for symptomatic relief of pain and muscle spasms. Injection Trigger point injections for symptoms of myofascial pain n Cervical epidural steroid injections for radicular symptoms have been shown to provide short-term symptomatic relief. n Zygapophyseal (facet) joint injections and radiofrequency neurotomy have been shown to provide pain relief. n

n n

60% to 80% of workers with neck will continue to have neck pain one year later. Workers with little influence over their job situation have a slightly poorer prognosis. General exercise is associated with a better prognosis. Less than half of patients with neck and shoulder pain will be free of pain after 1 to 5 years.

Helpful Hints n n

Review posture and workstation ergonomics Review the use of heavy shoulder bags

Suggested Reading Andersen JH, Kaergaard A, Frost P, et al. Physical, psychosocial, and individual risk factors for neck/shoulder pain with pressure tenderness in the muscles among workers performing monotonous, repetitive work. Spine. 2002;27(6):660–667.


n

105

Neck Pain in Athletes Description

Natural History

Neck pain in athletes encompasses mild to serious cervical injuries.

n

Variable

Diagnosis Etiology/Types n n n n n n n

Cervical strain or sprain Overuse injuries Cervical degenerative disc disease with or without radiculopathy Cervical spinal cord neurapraxia Stingers or burners Cervical compression/spinous process fractures Blunt trauma to the carotid artery

Epidemiology n

n n

Sporting activities are the second most common cause of neck pain after motor vehicle accidents presenting in the emergency department. Most commonly related to high-velocity contact sports Cervical strains and sprains are the most common injury.


Strains occur as eccentric stretch injuries within the substance or musculotendinous junction of the muscle Sprains involve a stretch injury to ligamentous structures. Spinous process fractures can occur from a strong muscle contraction. Cervical compression fractures are primarily due to hyperflexion. Blunt trauma to the carotid artery may cause dissection, thrombus, or emboli.

Risk Factors n n n

n

Football, hockey, wrestling, gymnastics Older age Preexisting spinal stenosis (cervical cord 3.5 mm of displacement between flexion and extension views or 11 degrees of rotation on an anterioposterior view indicates ligamentous laxity. n MRI is used for assessing cervical spinal cord injury or ligamentous injuries. n CT is used to better delineate bony anatomy. Pitfalls Passive range of motion should not be done on patients with a potential cervical cord injury n Missing associated ligamentous injury with a cervical compression fracture n

Clinical Features n

Clinical features are based on the mechanism of injury.

106

Neck Pain in Athletes

n n n n

Unconscious athletes are assumed to have cervical spinal cord injury until proven otherwise Witnessed spear tackling using the head may result in a spinal cord injury Severe cervical spasm Athlete apprehension Cervical pain with active range or motion

Treatment Medical If there is a possibility for a cervical injury, the neck needs to be immobilized with further workup in a nearby emergency room. n Cervical cord neurapraxia should be treated as a severe spinal cord injury. n Oral corticosteroids or NSAIDs for cervical radiculopathy n Compression fractures may be treated with a semirigid cervical collar for 8 to 10 weeks. n Spinous process fractures require a cervical collar for 4 to 6 weeks. n

Exercises Gentle range-of-motion exercises for most cervical strains, degenerative disc disease, or radiculopathy n Isometric strengthening n Sports-specific exercises or drills

Surgical n Indications for surgery include persistent or recurrent radicular symptoms, cervical myelopathy, and progressive neurologic deficit. n Stable one-level cervical fusions at C3 or below is not a contraindication for return to contact sports. n Two or three level cervical fusions without neurologic deficits should avoid contact sports. n More than a three-level fusion or a fusion above C3 is an absolute contraindication for return to contact sports. Consults Physical medicine and rehabilitation n Neurologic or orthopedic-spine surgery n

Complications of treatment n Persistent spinal cord injury

Prognosis n

n

Modalities n Heat, cold, ultrasound, and transcutaneous electrical nerve stimulation have been used for symptomatic relief of pain and muscle spasms. Injection n Epidural steroid injections for radicular symptoms

Return to sport following a cervical sprain or strain occurs when the athlete meets the following 3 criteria: – Is pain free – Can demonstrate full strength and range of motion – Has regained sports-specific neck function

Helpful Hints n

Unconscious athletes are assumed to have cervical spinal cord injury until proven otherwise.

Suggested Reading Zmurko MG, Tannoury TY, Tannoury CA. Cervical sprains, disc herniations, minor fractures, and other cervical injuries in the athlete. Clin Sports Med. 2003;22(3):513–521.


Red Flags n

107

Neck Strain Description

n

A neck strain results from an injury to the dynamic muscle stabilizers or static ligamentous structures of the neck.

n n

Etiology/Types n

May be associated with mechanical overload or a prolonged abnormal posture

Epidemiology n

Chronic strain or acute or repetitive neck injuries make up 85% of all neck pain complaints.


May be related to ligamentous or muscular injury from excessive tension or stretching Muscle fatigue from overuse Muscle spasm caused by muscle overload Paraspinal muscle deconditioning due to previous injury

Risk Factors n n n

Mechanical overload Muscle overuse Prolonged abnormal posture


Localized or diffuse nonradiating neck pain Worsened with abnormal posture May be associated with headaches

Natural History n n

Usually a self-limiting condition Recurrent episodes of increasing frequency and intensity are possible.

History Diffuse or localized tenderness with possible radiation into the shoulders, scapular region, occipital region, or anterior chest wall n Pain with neck range of motion n Worsens with activity and improved with recumbency n Dull, aching pain n

Exam Normal neurologic examination n Tenderness to palpation of paraspinal muscles n Decreased neck range of motion n

Testing n Laboratory tests are usually normal. n Plain radiographs are usually normal, although there may be enough muscle spasm to result in loss of the normal cervical lordosis. n Congenital abnormalities are rare in the cervical spine. n Unless indicated, advanced imaging studies will not clarify the diagnosis. Pitfalls Lack of correlation of the history to the physical examination n Overlooking a neoplasm n

Red Flags n n

Diagnosis Differential diagnosis n Herniated nucleus pulposus n Klippel–Feil syndrome describes patients with a congenital fusion of two vertebral bodies, several vertebral bodies, or the entire cervical spine. n Occipital neuralgia n Osteoarthritis n Posterior element fractures n Soft tissue or bony trauma n Spondyloarthropathies

108

Temporomandibular joint abnormalities with referral into the neck Tumors Torticollis

n

Neurologic changes Soft tissue or bony abnormalities may be an early sign of fracture or neoplasm. Skin rashes suggest a systemic illness.

Treatment Medical NSAIDs n Muscle relaxants n Short-term opioids n Limited use of a cervical collar, primarily at night n Acupuncture has been described as helpful for symptomatic relief. n

Neck Strain

Modalities n Heat, cold, ultrasound, and transcutaneous electrical nerve stimulation have been used for symptomatic relief of pain and muscle spasms. Injection Trigger point injections to block the reflexive spasm if 2 to 4 weeks have passed without significant improvement.

n

Neurologic or orthopedic-spine surgeon, if trauma was involved.

Complications of treatment Variable

n

Prognosis n n

Excellent chance of recovery over several weeks Pain may continue for months or years.

Helpful Hints n n

Generally a self-limiting condition The physician should reassure the patient that no damage will occur with continued activity.

n

Suggested Readings

Surgical Surgical intervention is possible for unstable spine.

Foye PM, Sullivan WJ, Sable AW, Panagos A, Zuhosky JP, Irwin RW. Industrial medicine and acute musculoskeletal rehabilitation. 3. Work-related musculoskeletal conditions: the role for physical therapy, occupational therapy, bracing, and modalities. Arch Phys Med Rehabil. 2007;88 (3 Suppl 1):S14–S17. Swezey RL. Chronic neck pain. Rheum Dis Clin North Am. 1996;22(3):411–437.

n

Consults Physical medicine and rehabilitation

n


Exercises n Minimal or no bed rest n Intermittent lightweight cervical traction to decrease spasms and pain n Physical activity within the patient’s pain tolerance n Physical therapy with a home exercise program focused on pain control and regaining mobility

109

Neurofibroma Description Neurofibroma is a common autosomal dominant syndrome of the central and peripheral nervous systems.

Etiology/Types n

n

Neurofibromatosis type I (peripheral neurofibromatosis) is the most common hereditary neoplastic syndrome, which is associated with a chromosome 17 defect. Neurofibromatosis type II, which is associated with acoustic neuromas, is due to a chromosome 22 defect.

History The initial presenting symptom is axial, radicular, or referred pain. n Worsened with recumbent positioning, sneezing, or a Valsalva maneuver n

Exam n Motor, sensory, and reflex changes may be noted. n Possible asymmetric signs of spinal cord injury may be present. n Spastic motor loss Testing X-rays may demonstrate erosion of the pedicle, intervertebral foramen widening, or vertebral scalloping. n Scoliosis occurs in 17% of patients. n Normal X-rays are consistent with an intradural tumor. n MRI may note multiple intradural and extramedullary masses n

Epidemiology n n

Incidence is 1 in 3,000 live births. Occurs in adults aged 30 to 60 years.

Pathogenesis n n

n

Arises from Schwann cells, fibroblasts, and nerve fibers 41% of cases affect the thoracic spine, 31% affect the lumbar spine, 26% affect the cervical spine, and 2% affect the sacrum. Can involve the sensory, motor, or combined sensorimotor portions of the nerve

Risk Factors n


Clinical Features n

n n

Clinical findings include neurofibromas, lisch nodules, café-au-lait spots, freckling, optic gliomas, and skeletal dysplasia. Adults typically present with kyphoscoliosis. A small number of patients may have no spinal abnormalities.

Natural History n n

3% of patients have malignant transformation. Malignant transformation is more likely in patients with multiple lesions.

Diagnosis Differential diagnosis n Meningioma n Schwannoma

110

Pitfalls Delay in diagnosis may range from 1 to 4 years.

n

Red Flags n

Signs of spinal cord compression

Treatment Medical Supportive

n

Exercises General conditioning exercises to prevent deconditioning

n

Modalities None

n

Injection None

n

Surgical Surgical resection is preferred for spinal cord or nerve root compression. n Resection is difficult with multiple lesions or intimacy with vital structures. n

Consults Physical medicine and rehabilitation n Neurologic or orthopedic-spine surgery n Neurology n

Neurofibroma

Prognosis n

Based on location of masses

Helpful Hints n

Important to assess for peripheral signs associated with neurofibromatosis

Suggested Readings Crawford AH, Parikh S, Schorry EK, Von Stein D. The immature spine in type-1 neurofibromatosis. J Bone Joint Surg Am. 2007;89 (Suppl 1):123–142. Ferner RE. Neurofibromatosis 1 and neurofibromatosis 2: a twenty first century perspective. Lancet Neurol. 2007;6(4):340–351. Savar A, Cestari DM. Neurofibromatosis type I: genetics and clinical manifestations. Semin Ophthalmol. 2008;23(1):45–51.


Complications of treatment Peripheral nerve injury n Spinal cord injury n Complications related to surgery n

111

Osteoblastoma Description Osteoblastoma is a rare, benign neoplasm of bone most commonly found in the lumbar spine.

Etiology/Types n

Unknown


Most common in individuals up to 30 years of age 3% of all benign bone tumors Male to female ratio is 2.5:1 Most common in the axial spine 50% of cases affect the lumbar spine. 38% of cases affect the cervical spine.

Pathogenesis n

Unknown

Risk Factors n

History Insidious localized dull, aching pain n Pain worsens with activity n Scoliosis n

Exam Characteristic localized tenderness with mild swelling over the involved spinal segment n Increased pain with extension of the spine n Neurologic findings associated with compression of the nerve roots or spinal cord n Positive straight leg raise has been found in 25% of patients n Muscle atrophy may be noted adjacent to the tumor n

Testing X-rays tend to be nonspecific; most common location is in the posterior elements with rare involvement of the vertebral body. n Rarely found to affect the atlas and axis n

Unknown

Clinical Features n

n n n n n n

Tumors tend to be 2 to 10 cm in length and made up of well-circumscribed hemorrhagic granular tissue Average duration of symptoms before diagnosis is 14 months. Insidious localized dull, aching pain overlying the involved bony segment Possible torticollis with cervical involvement Formation of scoliosis with thoracic or lumbar involvement Possible radicular pain associated with lumbar involvement Mass may encircle nerve roots

Natural History n

Progressive enlargement

Diagnosis Differential diagnosis n Giant cell tumor n Hyperparathyroidism n Osteoid osteoma n Osteosarcoma

112

Axial cervical T1-weighted magnetic resonance image with contrast and fat suppression demonstrating an osteoblastoma expanding into the right lamina (arrow). (Adapted from Fast A, Goldsher D. Navigating the Adult Spine: Bridging Clinical Practice and Neuroradiology. New York: Demos Medical Publishing, 2007:113.)

Osteoblastoma

n n n n

The mass tends to appear as a well-circumscribed lesion with a thin layer of bone surrounding a radiolucent or opaque center. Bone scan may be helpful in identifying a lesion that does not appear on X-rays CT allows for assessment of the extent of bony tumor penetration MRI allows for visualization of tumor penetration into the adjacent soft tissue. MRI with contrast is used periodically for focal enhancement of the mass.

Pitfalls Delay in diagnosis of months to years

n

Injection n None Surgical n Surgical excision of the tumor mass is the preferred method of treatment. n Partial curettage is used for masses that are inaccessible for full excision. Consults Neurologic or orthopedic-spine surgery n Radiation oncology n

Complications of treatment n Radiation therapy may result in malignant transformation, increased spinal cord compression, or necrosis

Red Flags n n

Progressive radiculopathy Spinal cord compression

Prognosis n n

Treatment Medical n Radiation therapy for lesions that cannot be completely excised n Radiation therapy may result in malignant transformation, increased spinal cord compression, or necrosis. n Chemotherapy has been found to slow the growth of the mass. Exercises n None Modalities None

n

n n n

Benign course Involvement of the axial spine is associated with greater morbidity and mortality. Pain resolves with complete excision. 5% recurrence rate Recurrence may occur up to 17 years.

Helpful Hints n n

Benign slow growing lesion Nerve root or spinal cord compression is possible.

Suggested Readings Kan P, Schmidt MH. Osteoid osteoma and osteoblastoma of the spine. Neurosurg Clin N Am. 2008;19(1):65–70. Zileli M, Cagli S, Basdemir G, Ersahin Y. Osteoid osteomas and osteoblastomas of the spine. Neurosurg Focus. 2003;15(5):E5.


n

113

Osteochondroma Description Osteochondroma is a common benign tumor of bone that may occur in a solitary location or in multiple locations.

Etiology/Types n

Thought to be related to abnormal cartilage growth during skeletal immaturity, which ceases growth once skeletal maturity has been reached


Makes up 36% of all benign bone tumors. 60% of patients are aged 30 or under, although it has been reported in older patients. Multiple lesions develop in patients before 20 years of age. Male to female ratio is 2:1

Pathogenesis n

Thought to be caused by a defect in the periosteal bone of the epiphyseal plate during embryogenesis

Risk Factors n

Unknown

Diagnosis Differential diagnosis n Callus associated with fracture n Chondroblastomas n Chondroid metaplasia n Chondromas n Malignant transformation n Osteophytes History Mild, deep pain n Pain improved with rest and worsened with activity n Painless palpable bony mass n Decreased joint range of motion n Possible motor, sensory, reflex changes n Possible bowel or bladder incontinence n

Exam May demonstrate no neurologic deficit, although there may be significant neurologic deficits associated with the level of involvement. n Tenderness with palpation of the mass n Decreased joint or segment range of motion n

Testing X-rays can be diagnostic, demonstrating protrusion of the mass on a sessile or bony stalk arising from the bone. n May be an incidental finding on X-rays of an asymptomatic patient n Bone scan demonstrates increased uptake at the site of the tumor n CT is used to demonstrate the size and location of the tumor and its relation to the bony and soft tissue structures. n MRI is not good at imaging the bony structure. n


Mild pain related to mechanical irritation of adjacent soft tissues Progression of pain over years Continued growth may result in decreased joint range of motion and function May result in scoliosis, radiculopathy, spinal stenosis, or cord compression

Natural History n

n n n n n n n n

Stops growing at skeletal maturity and is frequently asymptomatic, although with continued growth, it may lead to progressive neurologic compromise. Horner’s syndrome Brown-Séquard syndrome Sudden death Spinal cord injury Nerve root injury Occlusion of the vertebral artery Hoarseness Dysphagia

114

Pitfalls Patients should be monitored for changes in symptomatology or tumor size.

n

Red Flags n

Signs and symptoms of nerve root or spinal cord compression, which includes tetraparesis

Treatment Medical n None

Osteochondroma

Modalities None

n

Injection n None Surgical n Surgical decompression is required if there is neurologic compromise. Consults Neurologic or orthopedic-spine surgery

n


Prognosis n

Resolution of pain noted with surgical excision

n

Patients should be monitored as osteochondromas may become malignant.

Helpful Hints n

Monitoring patients for changes in the signs and symptoms of a symptomatic tumor

Suggested Readings Cooke RS, Cumming WJ, Cowie RA. Osteochondroma of the cervical spine: case report and review of the literature. Br J Neurosurg. 1994;8(3):359–363. Gille O, Pointillart V, Vital JM. Course of spinal solitary osteochondromas. Spine. 2005;30(1):E13–E19. Giudicissi-Filho M, de Holanda CV, Borba LA, Rassi-Neto A, Ribeiro CA, de Oliveira JG. Cervical spinal cord compression due to an osteochondroma in hereditary multiple exostosis: case report and review of the literature. Surg Neurol. 2006;66 (Suppl 3):S7–S11.


Exercises n None

115

Osteogenesis Imperfecta Description

Natural History

Osteogenesis imperfecta is a genetic disorder of connective tissue that results in decreased bone mass resulting in bony fragility.

n n

Multiple fractures Progressive scoliosis

Diagnosis Etiology/Types n n n n n n n

Type I: mild form, dominant inheritable form, most common Type II: lethal form resulting in perinatal death Type III: severe progressive form resulting in scoliosis and a short stature Type IV: moderate form Type V: variable severity, which may include radial head dislocation and interosseous calcification Type VI: moderate form Type VII: moderate to severe form, may result in intrauterine fractures

Epidemiology n

Prevalence is up to 1 in 5,000 individuals.

Pathogenesis n

n

Abnormal collagen maturation due to mutation of the two genes that encode collagen type 1 alpha chains (COL1A1 and COL1A2) Type I is autosomal dominant.

Differential diagnosis Achondrogenesis n Battered child syndrome n Idiopathic juvenile osteoporosis n Steroid-induced osteoporosis n

History Back pain due to vertebral body fractures and associated muscle spasm

n

Exam Blue sclera n Bony tenderness with associated muscle spasm n Scoliosis n Limb abnormalities due to previous fractures n

Testing X-rays note diffuse osteopenia with flattened vertebral bodies, “fish” vertebrae, and anterior wedging of the vertebral bodies.

n

Risk Factors n


Clinical Features Type I is associated with blue sclera, short to normal stature, variable bone fragility, and hearing loss. n Bone fragility increases in the following order: type I < types IV, V, VI, VII < type III < type II. n Short stature is the result of multiple fractures, bowing of the long bones, and kyphoscoliosis. n 80% of individuals develop scoliosis. n Ligamentous laxity n Otosclerosis n Premature vascular calcification n Constipation n Easy bruisability n Discoloration of teeth n Micrognathia n Temporal bulging 116 n

Posterioanterior chest plain radiograph demonstrating scoliosis and diffuse osteopenia characteristic in osteogenesis imperfecta. (Courtesy of Keith Hentel, MD.)

Osteogenesis Imperfecta

n

Radiographic evidence of six or more biconcave vertebrae prior to puberty indicates the progressive development of severe (>50-degree angle) scoliosis. CT and MRI may be useful in assessing for suspected vertebral body fractures not evident on plain radiographs.

Pitfalls Missed vertebral body fracture

n

Red Flags n

Missed vertebral body fracture

Treatment Medical NSAIDs and analgesics for pain n Intravenous pamidronate may be used to treat decreased bone density and pain. n Bracing does not prevent the progression of scoliosis. n

Exercises Focus on maximizing mobility and functional activities, although this can be severely limited in patients with severe bone fragility. n Exercise does not prevent the progression of scoliosis. n


Injection n None Surgical n Percutaneous vertebral augmentation for vertebral body-compression fractures n Spinal fusion for scoliosis >50 degrees to halt the loss in pulmonary function Consults Neurologic or orthopedic-spine surgery n Rheumatology n

Complications of treatment n Complication rates approach 50% with surgical management of scoliosis.

Prognosis n

Pulmonary compromise is the primary cause of death in patients with a thoracic scoliosis of 60 degrees or greater.

Helpful Hints n

Focus on maximizing mobility and functional activities

Suggested Readings Engelbert RH, Pruijs HE, Beemer FA, Helders PJ. Osteogenesis imperfecta in childhood: treatment strategies. Arch Phys Med Rehabil. 1998;79(12):1590–1594. Rauch F, Glorieux FH. Osteogenesis imperfecta. Lancet. 2004;363(9418):1377–1385.


n

117

Osteoid Osteoma Description

n

Osteoid osteoma is a painful, benign primary bone tumor.

n n

Etiology/Types n

Unknown


Makes up 12% of all benign tumors. Most common between the ages of 20 and 30 years 18% are located in the axial spine. 44% of these affect the lumbar spine and 30% affect the cervical and thoracic spines. Male to female ratio is 2:1

Pathogenesis n

Theories include a consequence of a chronic infection or reparative process or a benign bone neoplasm with limited growth potential.

Risk Factors n

n n

Lumbar strain Metastasis Osteoblastoma Osteomyelitis Osteosarcoma

History n Vague intermittent pain with increasing intensity n Pain characteristically improved with aspirin or NSAIDs. n Pain is worse at night. n Pain not improved with heat or rest. n Possible radicular symptoms Exam Tenderness over the involved bony structure n A progressive scoliosis may be related to asymmetrical muscle spasm. n Superficial presentation may result in swelling and erythema. n Sensory changes are rare. n

Unknown

Clinical Features n

n n n n

Pain that is relieved with aspirin or NSAIDs is the characteristic feature, although some osteoid osteomas may not be painful or may not respond to antiinflammatory drugs. An initial manifestation may be scoliosis. Osteoid osteoma of the cervical spine is only found in the pedicles and the posterior elements. Cervical presentation may include torticollis and occipital headache. 75% of presentations occur in the neural arch, 18% occur at the zygapophyseal (facet) joints, and 7% occur in the vertebral body.

Natural History n n

Generally described as increasing pain Irreversible scoliosis

Diagnosis Differential diagnosis n Eosinophilic granuloma n Ewing’s sarcoma n Fracture n Herniated nucleus pulposis

118

Axial CT of the C4 vertebrae with a sclerotic nidus at the laminar-pedicle junction (arrow) characteristic of an osteoid osteoma. (Adapted from Fast A, Goldsher D. Navigating the Adult Spine: Bridging Clinical Practice and Neuroradiology. New York: Demos Medical Publishing, 2007:113.)

Osteoid Osteoma

Pitfalls Several years may pass before a diagnosis is made. n In skeletally immature patients, scoliosis may result in permanent scoliosis. n Skeletally mature patients may have resolution of their scoliosis with surgical excision of the tumor. n

Red Flags n

n

Low back pain that worsens at night and is improved with aspirin in a young healthy adult may be mislabeled as psychogenic or malingering. Rare radicular symptoms

Treatment Medical NSAIDs may be used for symptom control.

n

Exercises None

n

Modalities n None Injection n None Surgical n Excision of the nidus and surrounding sclerotic bone may result in pain relief. n Radiofrequency abalation may also be used to resolve the clinical symptoms. Consults Neurologic or orthopedic-spine surgery

n


Prognosis n n n

Recurrence is possible with incomplete excisions up to 10 years. Spontaneous resolution has been reported in the literature. No known cases of malignant transformation have been reported.

Helpful Hints n

Full resection of the tumor can correct preoperative scoliosis and associated paraspinal muscle spasm.

Suggested Readings Kan P, Schmidt MH. Osteoid osteoma and osteoblastoma of the spine. Neurosurg Clin N Am. 2008;19(1):65–70. Lee EH, Shafi M, Hui JH. Osteoid osteoma: a current review. J Pediatr Orthop. 2006;26(5):695–700.


Testing X-rays can diagnose osteoid osteoma based on the characteristic surrounding area of dense sclerotic bone enclosing a radiolucent center that is 1.5 cm in diameter. n May be difficult to detect on X-rays n Bone scan demonstrates regions of tumor with increased activity. n X-rays may also be used to monitor for local tumor recurrence. n CT is used to determine the extent of bony involvement. n CT-guided percutaneous biopsy may be used to resect accessible lesions. n MRI is not routinely used. n

119

Osteomyelitis, Vertebral Body Description

Natural History

Vertebral osteomyelitis refers to the growth of organisms within the bony structures of the axial spine.

n n

Etiology/Types n

Common organisms include Staphylococcus aureus, Escherichia coli, Brucella abortus, Mycobacterium tuberculosis, Coccidiodes immitis, Treponema pallidum, and Echinococcus granulosus.


Incidence is estimated at 1 in 250,000. Up to 4% of all cases of osteomyelitis involve the vertebral body. The mean age is 45 to 62 years. The lumbar spine is the most commonly affected site followed by the thoracic spine, cervical spine, and sacrum.


Usually the result of hematogenous spread through Batson’s plexus. May also occur through direct inoculation from interventional or surgical procedures. Vertebral body infection may spread into the adjacent soft tissue. The most common organism is Staphylococcus aureus.


Alcoholism Chronic disease such as renal failure, HIV, and malignancy Dental extraction Genitourinary tract infection Infective endocarditis Intravenous drug use (Pseudomonas aeruginosa) Soft tissue infection Surgery: 1% for discectomy, and 6% for instrumented fusion


Bacterial infections result in acute toxic reactions. Fungal or tuberculous infections are indolent reactions.

120

Generally the pain develops over 8 to 12 weeks before the diagnosis is made. Progression of the infection may involve the surrounding soft tissues.

Diagnosis Differential diagnosis Discitis n Metastatic tumors n Multiple myeloma n Sarcoidosis n

History History of a recent interventional procedure or surgery n Spinal pain corresponding to the level of involvement n Constant or intermittent pain n Pain improves with rest and worsens with motion. n 30% may demonstrate radicular symptoms. n Sore throat or dysphagia may occur with cervical involvement. n

Exam Fever n Decreased spinal range of motion n Tenderness over the involved spinal segment n A psoas abscess may present with a hip flexor “contracture.” n Cervical presentation may include Horner’s syndrome and torticollis. n Possible neurologic deficits n

Testing During the acute phase, the white blood cell count and the erythrocyte sedimentation rate may be elevated n The most useful test is direct culture of the blood and bony lesion. n X-ray changes are delayed up to 2 months. n Characteristic changes on X-rays include loss of vertebral body definition, bone loss, and narrowing of the disc space. n Bone scan is positive earlier, within 72 hours after the onset of infection. n SPECT may allow clearer visualization of infection within the posterior elements. n CT demonstrates bony changes and penetration into the soft tissues n

Osteomyelitis, Vertebral Body

n n

121

by an oral course as long as 6 months, depending on the organism. Immobilization Bed rest

Exercises n None Modalities n Modalities are contraindicated as they may increase the spread of the infectious process. Injection None

Surgical n Decompression and fusion may be required for patients who develop spinal instability. Consults Infectious disease n Neurologic or orthopedic-spine surgery n

Sagittal thoracic T2-weighted magnetic resonance image with fat suppression demonstrates osteomyelitis of adjacent vertebral bodies with complete destruction of the intervertebral disc. (Courtesy of Keith Hentel, MD.)

n

MRI is very sensitive in demonstrating the inflammatory process within the bony structure and surrounding soft tissue structures.

Complications of treatment n Bony destruction may cause spinal instability. n Spinal cord injury n Complications related to delay in diagnosis, antibiotics, or surgical treatment

Prognosis n

With early diagnosis and treatment, the patient will have minimal disability. Up to 10% of patients have a relapse with inadequate treatment.

Pitfalls n Delayed diagnosis

n

Red Flags

Helpful Hints

n n

Progressive spinal instability Progressive neurologic compromise

Treatment Medical n Antibiotic choice is governed by the culture results and may require up to 6 weeks of treatment followed

n n

Diagnosis is often missed. Mycobacterial osteomyelitis may take up to 3 years before a diagnosis is made.

Suggested Reading Concia E, Prandini N, Massari L, et al. Osteomyelitis: clinical update for practical guidelines. Nucl Med Commun. 2006;27(8):645–660.


n

Osteoporosis Description Osteoporosis is characterized by increased bone fragility and fractures resulting in increased morbidity and mortality.

Etiology/Types n

Deterioration of the bone matrix leading to bone fragility

Epidemiology n n n

20% of white postmenopausal women in the United States have osteoporosis. One out of every two white women will experience an osteoporotic fracture at some point in her lifetime. The incidence of osteoporosis is lower in men due to larger bone mass and size, shorter lifespan, and the lack of a male menopausal state.

Pathogenesis n

Caused by decreased estradiol after menopause in females and age-related bone metabolism changes as well as increased osteoclastic bone resorption, endocortical thinning, and an increasingly porous cortex

History Inciting event n Pain is improved with supine positioning. n Worsens with walking or sitting n

Exam Bony tenderness at the fracture site n Associated paraspinal muscle spasm n Step-off deformity of the spinous processes n Myelopathy due to retropulsion of the bony fragments into the central spinal canal n Asymmetric leg positioning while supine n Asymptomatic vertebral body compression fractures suspected with loss of >1.5 inches in serial height measurements or if the ribs touch the iliac crests n

Testing Urine calcium, serum thyrotropin, protein electrophoresis, cortisol, or anti-gliadin IgA and IgG antibodies to assess for celiac disease n Older patients should be assessed for osteomalacia with a check of the 25-hydroxyvitamin D level. n


Chronic obstructive pulmonary disease Eating disorders Female gender/athletic triad Gastrectomy Hyperparathyroidism Increasing age Low bone-mineral density Low body weight (70 degrees may have continued progression after skeletal maturity. Continued kyphosis may result in continued back pain

Helpful Hints n

In skeletally immature patients, it is important to follow the kyphotic progression.

Suggested Readings Kapetanos GA, Hantzidis PT, Anagnostidis KS, Kirkos JM. Thoracic cord compression caused by disk herniation in Scheuermann’s disease: a case report and review of the literature. Eur Spine J. 2006;15(Suppl 5):553–558. Lonner BS, Newton P, Betz R, et al. Operative management of Scheuermann’s kyphosis in 78 patients: radiographic outcomes, complications, and technique. Spine. 2007;32(24):2644–2652.


Treatment

141

Schwannoma Description

n

A schwannoma is a solitary benign Schwann cell tumor that is found on sensory nerve roots.

n

Etiology/Types n

Thought to arise from Schwann cells at the dorsal roots, the anterior spinal artery, or aberrant intramedullary nerve fibers

n

Meningioma Neurofibroma Spinal stenosis

History Pain n Motor and sensory changes n

Exam Motor and sensory deficits

n


Prevalence unknown Make up to 35% of all primary intraspinal tumors Occur in patients between 30 and 40 years of age 30% occur in the lumbar region. No gender preference More common in the cervical and lumbosacral regions

Testing n MRI is used for early diagnosis and prognosis. n CT n CSF demonstrates increased protein. Pitfalls Misdiagnosis n Typically there is no change with discectomy. n

Red Flags n

None acutely

Pathogenesis n n n

Commonly benign Encapsulated and typically round tumors that are attached to the nerve root. Vascular supply may originate from branches of the anterior spinal artery

Risk Factors n

Unknown


Neurologic dysfunction No pain initially, but pain usually develops Pain worsens with recumbent positioning Sensory or motor dysfunction related to a spaceoccupying lesion May occur in the cervical spine or sacrum May eventually erode the vertebral body, pedicles, or foramen

Natural History n

Slow growing

Diagnosis Differential diagnosis Herniated nucleus pulposus

n

142

Sagittal T1-weighted magnetic resonance image with contrast demonstrating a schwannoma at the C7–T1 level (arrow). (Adapted from Fast A, Goldsher D. Navigating the Adult Spine: Bridging Clinical Practice and Neuroradiology. New York: Demos Medical Publishing, 2007:115.)

Schwannoma

Treatment

n

Medical n None

n

Modalities None

n

Injection n None Surgical n Resection possible n Radiation therapy Consults Neurologic or orthopedic-spine surgery n Radiation oncology n

Complications of treatment Continued neurologic dysfunction following surgical resection

n

Spinal instability related to surgical resection Arachnoiditis with surgery

Prognosis n

Usually excellent recovery following a complete resection, although there is a risk of recurrence.

Helpful Hints n

Possible misdiagnosis

Suggested Readings Conti P, Pansini G, Mouchaty H, Capuano C, Conti R. Spinal neurinomas: retrospective analysis and long-term outcome of 179 consecutively operated cases and review of the literature. Surg Neurol. 2004;61(1):34–43. Guyer RD, Collier RR, Ohnmeiss DD, et al. Extraosseous spinal lesions mimicking disc disease. Spine. 1988;13(3):328–331. Nicoletti GF, Passanisi M, Castana L, Albanese V. Intramedullary spinal neurinoma: case report and review of 46 cases. J Neurosurg Sci. 1994;38(3):187–191.


Exercises None

n

143

Scoliosis Description

n

Scoliosis is a lateral curvature of the spine greater than 10 degrees.

n n n

Etiology/Types

n

Functional scoliosis reduces to normal with forward bending. n Kyphoscoliosis describes a lateral curvature with an increased sagittal angulation. n Major categories of adult scoliosis – Individuals younger than 40 years without degenerative changes with scoliosis since adolescence – Individuals older than 40 years with degenerative changes – Elderly individuals who develop scoliosis due to degenerative changes of the thoracolumbar spine n More than 90% of cases are of an unknown etiology.

n

n

n n n n

Extraspinal or hip contractures Leg-length discrepancy Metabolic disorders Nerve root irritation/postural Neuromuscular diseases Osteomalacia Osteoid osteoma Rheumatoid disease Trauma Tumors

History Increasing pain just below the apex of the curve n Pain worsens with activity and improves with recumbency. n Family history of scoliosis n Unequal trouser-leg lengths n

Exam Focus is on shoulder, scapular, and pelvic asymmetry or obliquity as well as leg-length discrepancy. n Neurologic evaluation to assess for possible nerve root compression n Pulmonary evaluation should be followed for severely scoliotic patients. n

Epidemiology n n n

Found in up to 7.5% of individuals Prevalence increases with age. Increased female prevalence with curves >20 degrees

Pathogenesis n

Generally unknown

Risk Factors n n n

Compression fractures related to osteoporosis Osteoarthritis Possibly genetically related

Clinical Features n

n

Pain may be related to zygapophyseal (facet) degeneration, nerve root impingement on the concave side, or rib impingement on the iliac crest. Pain worsens with curve progression

Natural History n

A lumbar curve in a skeletally mature individual 40 degrees will progress 1 degree per year.

Diagnosis Differential diagnosis n Congenital diseases

144

Testing Full-length anterior–posterior and lateral thoracolumbar X-rays n The Cobb method is used to measure the angle of lateral spinal curvature by measuring the angle between two intersecting perpendicular lines that originate from the superior endplate of the upper vertebral body and the inferior endplate of the inferior vertebral body. n Progression is noted if there is an increase of >5 degrees in the curvature compared to previous films. n CT and MRI are limited to patients with suspected nerve root involvement or in surgical planning. n Pulmonary testing n

Pitfalls Missing a reversible cause of scoliosis such as an osteoid osteoma or a leg-length discrepancy

n

Red Flags n n

Continued progression of the scoliotic curve Pulmonary compromise

Scoliosis

145

Surgical n Indicated for progression of scoliosis in patients younger than 40 years if the curve is >50 degrees. n In those aged 40 years and older, indications include progression, radicular pain, and pulmonary compromise. n Surgery can restore function in patients. n Important to assess bone density during preoperative surgical planning Consults Physical medicine and rehabilitation n Neurologic or orthopedic-spine surgery (clinicians with extensive experience with scoliosis surgery) n

Coronal computed tomography scout film demonstrating severe scoliosis.

Treatment

Complications of treatment n Surgical risks include pseudoarthrosis, infection, and the development of curvature above the fusion.

Medical n Heel lift for patients with leg-length discrepancies n Analgesics n NSAIDs n Milwaukee brace for adolescents

Prognosis

Exercises General strengthening and stretching exercises n Yoga has been found to be helpful.

Helpful Hints


Suggested Reading

n

n

n

n

Increased morbidity and mortality with untreated severe scoliosis due to increased pain and pulmonary compromise

A lumbar curve in a skeletally mature individual >40 degrees will progress 1 degree per year.

Lonstein JE. Scoliosis: surgical versus nonsurgical treatment. Clin Orthop Relat Res. 2006;443:248–259.


Injection n Zygapophyseal (facet) joint injections for zygapophyseal (facet) joint pain n Medial branch block testing followed by radiofrequency denervation of the medial branch associated with zygapophyseal (facet) joint pain n Epidural steroid injection for radicular symptoms

Spinal Cord Injury Description

n

Spinal cord injury results in the loss of motor and/or sensory function below the level of injury resulting in loss of function of the caudal limbs with bowel and bladder deficits.

n


Etiology/Types n

n n n

n

Etiology includes motor vehicle accidents, falls, sports, violence, vascular disorders, infectious causes, vertebral body compression fractures, developmental disorders, and tumors. Complete injury describes the loss of motor and sensory function in the lowest sacral segments. Incomplete injury describes preservation of sensory and/or motor functions below the level of injury. Tetraplegia describes loss of motor and/or sensory function within the cervical spinal cord resulting in impaired function of the arms, trunk, pelvic organs, and legs. Paraplegia describes loss of motor and/or sensory function within the spinal cord in the thoracic or lumbar spinal cord or sacral nerve roots resulting in impaired function in the trunk, pelvic organs, and legs.

Unemployment Violence

n n

Based on presenting level of injury Spinal shock lasts an average of 3 weeks and is thought to be due to the interruption of the descending excitatory fibers resulting in the loss of the reflex arc with flaccid muscles. Loss of bulbocavernosus reflex during the period of spinal shock Increased reflexive activity following spinal shock results from the loss of the descending inhibitory impulses.

Natural History n

Functional outcome is based on the level of injury.

Diagnosis Differential diagnosis None for trauma-related spinal cord injury

n


12,000 new cases per year in the United States Average age of injury is 39.5 years Male to female ratio 4:1 42% of all injuries result from motor vehicle accidents. 23.8% of all injuries result from falls. Falls are the most common cause of injury in people over the age of 60.

Pathogenesis n

Kinetic energy of the injury or trauma causes spinal cord compression with neuronal and vascular injury followed by hemorrhage, inflammation, and ischemia resulting in further damage to the spinal cord.


Caucasian ancestry Falls in the elderly population Fewer years of education Male gender Motor vehicle accidents/diving Single

146

Sagittal cervical T2-weighted magnetic resonance image with fat suppression demonstrating increased signal within the spinal cord at the C0–C2 level (arrow) following a fall from a fifth storey building. (Courtesy of Keith Hentel, MD.)

Spinal Cord Injury

147

History Associated injury or trauma with loss of function of the upper or lower extremities with bowel and bladder dysfunction

Surgical n Optimal timing for surgery is believed to be within 24 hours of injury.

Exam n Based on American Spinal Injury Association (ASIA) classification

n

Testing Appropriate MRI or CT to assess trauma or injury n Electrodiagnostic studies to rule out peripheral nerve injury n

Pitfalls The physical examination is most accurate 72 hours post-injury, allowing for an initial prognosis. n Hypercalcemia n

Red Flags n

Missed fractures, peripheral nerve injuries, and traumatic brain injury

Treatment Medical n Differentiation of neurogenic shock from hypovolemic shock n Early traction for cervical fractures n Intravenous methylprednisolone n Assessment of skin with frequent positioning n Indwelling urinary catheter Exercises n Range of motion exercises as the patient recovers from spinal shock to prevent contractures

Consults Physical medicine and rehabilitation n Neurologic or orthopedic-spine surgery Complications during acute rehabilitation n Autonomic dysreflexia n Orthostatic hypotension n Bowel and bladder dysfunction n 16% to 53% of patients develop heterotropic ossification. n 47% to 100% of patients develop a deep vein thrombosis. n 11% to 94% of patients develop pain. n Gastric atony and ileus in the acute phase n Pneumonia/pulmonary embolism n Spasticity n Pressure ulcers

Prognosis n

n

n n

Prognosis is most accurate after 72 hours, after which a complete injury rarely becomes an incomplete injury. Preservation of pinprick sensation below the level of injury at 72 hours postinjury increases the chances of progression to ASIA status D or E. Patients with complete tetraplegia may regain at least one motor level within the first 1 to 2 years. Patients with three-fifths of quadriceps strength at 2 months postinjury may walk by 1 year postinjury.

Helpful Hints n

The physical examination is most predictive within 72 hours of injury.


Suggested Reading

Injection n None in the acute setting

Branco F, Cardenas DD, Svircev JN. Spinal cord injury: a comprehensive review. Phys Med Rehabil Clin N Am. 2007;18(4):651–679.


n

Spinal Stenosis, Cervical (Cervical Myelopathy) Description

Diagnosis

Cervical spinal stenosis is the most common spinal cord dysfunction in the older population and is the most common cause of nontraumatic spastic paraparesis and tetraparesis.

n

Etiology/Types n

Extensive degenerative changes in the axial spine can cause spinal cord ischemia at one or more levels.

Epidemiology n

Unknown

Pathogenesis n

n

n

Spondylotic changes result from disc degeneration increasing mechanical stress at the endplates of adjacent vertebral bodies with the development of osteophytic spurs. Osteophytic spurs increase the weight-bearing surface of the endplates stabilizing the adjacent vertebrae and decreasing the hypermobility, which results from disc degeneration. With cervical flexion, the spinal cord lengthens and is stretched over the ventral osteophytic bars.

Risk Factors n n n

Congenital central stenosis Down syndrome Repeated occupational trauma

Clinical Features n n n n n n n

Gait abnormality Lower-extremity weakness and spasticity No pain associated with progression Loss of manual dexterity Triceps and/or hand intrinsic weakness is common in the upper extremity. Iliopsoas and quadriceps muscle weakness is common in the lower extremities. Changes in bowel or bladder function may occur at later stages.

Natural History n

Slow and insidious progression of symptoms

148

Differential diagnosis Amyotrophic lateral sclerosis n Multiple sclerosis n Polyneuropathy n Primary lateral sclerosis n Radiculopathy n Rheumatoid arthritis n Spinal arteriovenous malformations n Spinal cord tumor n Syringomyelia n Tabes dorsalis History n Upper- or lower-extremity weakness, numbness, or tingling n Difficulty with fine motor control n Gait abnormality due to lower extremity weakness and/or proprioceptive deficits Exam Lhermitte’s sign resulting in electrical shocks down the trunk and extremities with flexion of the cervical spine n Fixed neck flexion n Weakness in affected dermatomes n

Testing X-rays can be difficult to interpret as cervical spondylotic changes increase with aging. n An anterior–posterior canal diameter of 50%) n Pain worsens with activity and improves with rest n

Exam Positive stork test or single-leg standing hyperextension test n Flattened lumbar lordosis with muscle spasm n Pelvic waddle gait described as a stiff-legged gait with short strides n Dural root tension signs n Palpable step-off deformity n

Testing Oblique X-rays demonstrate a broken neck or collar of the “Scotty dog” confirming a pars interarticularis fracture. n Flexion extension X-rays are useful to asses for anterior–posterior instability. n Lateral X-rays are useful to assess the degree of translation, the sacral inclination, slip angle. n Instability is considered with slips on lateral X-rays of >50%. n SPECT can localize the level of the lesion, and increased activity suggests healing potential. n Thin-cut tomography may demonstrate the fracture and is useful for follow-up evaluations. n

Spondylolysis/Spondylolisthesis, Lumbar n n

157

NSAIDs Spinal orthosis

Exercises n Hip flexion and hamstring contracture stretching n Core lumbar stabilization Modalities n Heat, cold, ultrasound, and transcutaneous electrical nerve stimulation have been used for symptomatic relief of pain and muscle spasms. Injection Blocks of the pars interarticularis may be helpful in diagnosis and treatment.

Surgical L5–S1 fusion with autologous posterior iliac crest bone graft for symptomatic L5 spondylolysis n Decompression is considered in patients with radiculopathy or bowel or bladder dysfunction. n

Lateral lumbar plain radiograph demonstrating a grade 1 anterolisthesis and a defect in the pars interarticularis (arrow) at the L5–S1 level. (Adapted from Fast A, Goldsher D. Navigating the Adult Spine: Bridging Clinical Practice and Neuroradiology. New York: Demos Medical Publishing, 2007:56.)

n

MRI to evaluate for a stress response and potential radiculopathy

Pitfalls Diagnostic difficulty for spondylolysis

n

Red Flags n

Neurologic compromise

Treatment Medical n Cessation of sporting activities

Consults Physical medicine and rehabilitation n Neurologic or orthopedic-spine surgery n

Complications of treatment n Complications related to injection and surgery

Prognosis n n n

Patients may heal spontaneously Patients with symptoms should refrain from heavy lifting or high-level athletic activities. No heavy lifting or high-level athletic activities following surgical fusion

Helpful Hints n

Assessment for neurologic compromise

Suggested Reading Hu SS, Tribus CB, Diab M, Ghanayem AJ. Spondylolisthesis and spondylolysis. J Bone Joint Surg Am. 2008;90(3):656–671.


n

Spontaneous Epidural Hematoma Description

n

Acute bleeding into the epidural space of the spinal canal

n n

Bowel or bladder dysfunction Symptoms may progress from minutes to hours. Other presentations include slowly progressive, chronic, and relapsing symptoms.


Most occur spontaneously Acute bleeding from an extradural vessel or the posterior epidural venous plexus Chronic types are rare and typically occur in the cervical spine.


Spontaneous hematomas account for up to 50% of all spinal epidural hematomas. Most common in patients 50 to 80 years of age Most common in the cervicothoracic spine, followed by the thoracolumbar spine Cervical spine more commonly involved in children and young adults Male to female ratio is 1.5:1


The lumbar spine is better able to accommodate to an expanding mass due to its larger diameter. Extends for at least two or more segments Found most commonly in the posterolateral position Sudden nerve root or spinal cord compression Sudden compression of the anterior spinal artery

Risk Factors n n n n n n n n n n n

Anticoagulation Arteriovenous malformations Chiropractic spinal manipulation Cocaine use Hemophilia Leukemia Myelography Spinal procedures Spondylosis Surgery Thrombocytopenia


Sudden and severe neck or back pain Radicular pain Neurologic dysfunction

158

Natural History n

Sudden and progressive radiculopathy or spinal cord injury

Diagnosis Differential diagnosis Epidural abscess n Intervertebral disc herniation n Lumbar spinal stenosis n

History Initial symptoms may be vague n Sudden and severe neck or back pain n Motor and sensory dysfunction n Bowel or bladder dysfunction n

Exam Motor and sensory dysfunction n Bowel or bladder dysfunction n

Testing n MRI demonstrates a mass that is isodense on T1-weighted images with increased signal on T2-weighted images within the first 24 hours. After 24 hours, there is high T1-weighted signal and low T2-weighted signal. n MRI with contrast may demonstrate peripheral enhancement or occasional central enhancement. Pitfalls Delayed treatment

n

Red Flags n n

Progressive motor and sensory dysfunction Bowel or bladder dysfunction

Treatment Medical n Indicated with mild presentations, serious coagulopathy, high operative risks, or prolonged paralysis n Anticoagulated patients may receive vitamin K and fresh frozen plasma.

Spontaneous Epidural Hematoma

n

n

Platelet transfusion with thrombocytopenia Treatment of coagulopathy may prevent progression of the hematoma and allow for nonoperative treatment as some believe that the hematoma remains as liquid longer in patients with coagulopathies, allowing it to spread further along the epidural space. Cervical epidural hematoma may respond to neck immobilization and steroid administration.

Exercises n None Modalities None

Prognosis n

n

n n n n

n

Injection n None Surgical Emergent decompressive laminectomy with hematoma evacuation is considered with neurologic dysfunction.

n

Consults n Neurologic and orthopedic-spine surgery Complications of treatment Radiculopathy n Spinal cord injury n Death n

n

Best outcomes are observed if the surgery is completed within 36 hours with complete SCI injuries and ≤48 hours with incomplete SCI injuries. Based on extent of the hematoma, the preoperative neurologic deficits, and the time interval between symptom onset and surgical decompression Lumbar hematomas have the best prognosis. Cervical and thoracic hematomas have a poorer outcome. Incomplete sensory and motor deficits suggest a good postoperative recovery. Preoperative absence of sensorimotor function does not indicate a poor outcome. Cervical or cervicothoracic presentations may favor spontaneous recovery.

Helpful Hints n

Always include a spontaneous epidural hematoma in the differential of acute neck or low back pain.

Suggested Readings Liu WH, Hsieh CT, Chiang YH, Chen GJ. Spontaneous spinal epidural hematoma of thoracic spine: a rare case report and review of literature. Am J Emerg Med. 2008;26(3):384.e1–2. Groen RJ. Non-operative treatment of spontaneous spinal epidural hematomas: a review of the literature and a comparison with operative cases. Acta Neurochir (Wien). 2004;146(2):103–110.


n

159

Stingers and Burners Description

n

Stingers and burners describe cervical nerve root or brachial plexus injuries resulting in shoulder and upperextremity pain, dysesthesias, and weakness.

n

Etiology/Types

n

Associated weakness, numbness, or tingling is found in the affected dermatome Neck pain is uncommon.

Natural History n n

n

n

Traction: lateral neck flexion to the contralateral side with ipsilateral shoulder depression Compression: shoulder pad compression of the brachial plexus against the superior medial scapula at Erb’s point Hyperextension with or without lateral flexion: nerve root compression within the intervertebral foramen Shoulder distraction away from the neck or forced oblique neck extension

Epidemiology n n

Thought to be the most common injury in sports medicine, although commonly under-reported 18% to 65% of collegiate football players experience this condition.

n

Usually self-limiting, lasting from seconds to weeks Some cases may lead to persistent subtle neurologic deficits or complete loss of affected extremity function.

Diagnosis Differential diagnosis Cervical fracture n Cervical sprain or strain n Clavicle fracture n Zygapophyseal (facet) joint dislocation n Intervertebral disc injury n Spinal cord injury n Thoracic outlet syndrome with medial or lower cord changes of the brachial plexus n

History Burning pain and dysesthesias along a dermatomal pattern n Shoulder abduction relief sign n

Pathogenesis C5 and C6 anterior rami make up the upper trunk and converge at Erb’s point making it the most commonly injured region. n Cervical nerve roots are susceptible to injury due to – lack of a protective epineurium, perineurium – dural dentate ligaments that anchor roots – compression of the nerve roots between the vertebral artery and the transverse process or due to scalene muscle hypertrophy. n C4–C5 and C5–C6 foramen are most commonly affected. n


Basketball, boxing, weightlifting, rugby Degenerative changes of the cervical spine Football is the most common cause. Wrestling is the second most common cause.

Clinical Features n

n

Stinging or burning-type pain radiating with possible weakness affecting the shoulder down the upper limb to the hand Athletes shake affected hand

160

Exam Rule out possible head injury or spinal cord injury n Removal of sporting equipment if appropriate n Assess for swelling, tenderness or deformity n Active neck range of motion n Gentle Spurling’s maneuver n Motor, sensory, and reflex testing n Assess acromioclavicular joint, glenohumeral joint, and supraclavicular region deformity n Tinel’s sign at Erb’s point n Slightly flexed cervical spine posture to decrease pressure within the neuroforamen n

Testing n X-rays of the cervical spine n Three times greater risk of a burner with a Torg/ Pavlov ratio of 1.5 cm in diameter and patients present with radicular pain. n Lumboperitoneal shunt for continuous CSF drainage n Decompressive laminectomy has a low success rate. n Cyst or nerve root excision leads to significant morbidity. n Microsurgical cyst fenestration and imbrication with improvement noted up to 17 months Consults Physical medicine and rehabilitation n Neurologic or orthopedic-spine surgery n

Treatment

Complications of treatment n Potential for recurrence following surgery n Poor surgical outcomes

Medical NSAIDs

Prognosis

Exercises n Pelvic stabilizers and abdominal muscle strengthening n Hamstring stretching

Helpful Hints

n


n

n

n

Injection n Lumbar CSF drainage to decrease CSF pressure and cystic pressure, although symptoms may return once drainage is stopped.

n

Variable

Although most commonly asymptomatic, Tarlov cysts should be considered in a differential diagnosis if other causes have been ruled out. Symptoms worsen with standing, coughing, or Valsalva maneuver

Suggested Reading Nadler SF, Bartoli LM, Stitik TP, Chen B. Tarlov cyst as a rare cause of S1 radiculopathy: A case report. Arch Phys Med Rehabil. 2001;82(5):689–690.


Testing n X-rays may demonstrate erosion of the sacrum, and rounded paravertebral shadow n MRI demonstrates CSF-like characteristics, low T1-weighted and high T2-weighted images; may also demonstrate bone and pedicle erosion, neuroformaminal enlargement, or sacral canal widening n CT demonstrates isodense lesions compared to CSF and bony erosions n CT myelography may demonstrate a delayed filling pattern of one hour with water-soluble contrast n Myelography may demonstrate a characteristic delayed filling pattern. n Electrodiagnostic studies to assess for radiculopathy

167

Tethered Cord Syndrome Description

n

Stretching or tethering of the spinal cord resulting in a traction neuropathy is caused by inelastic structures that may include a fibroadipose filum terminale, myelomeningocele, lipomyelomeningocele, scar tissue, or a bony spicule. First described by Garceau as filum terminale syndrome in 1953.

n

Etiology/Types

n

n n

Childhood onset is most common. Adult delayed onset may be due to cumulative effects of oxidative metabolism impairment, progressive increased filum terminale fibrous tissue with aging, sudden stretching of the spinal cord, or age-related spondylitic changes that exacerbate stretching of the spinal cord.

Epidemiology n

Unknown

Pathogenesis n

n

Oxidative metabolism impairment due to constant stretching of the spinal cord with resulting decreased regional blood flow Neuronal membrane changes

Risk Factors n

Spinal dysraphism

Clinical Features n

n n n n n n n n n n

Lower back pain and leg pain that is exacerbated with physical activity, particularly lumbar flexion and extension. Groin pain Genitorectal pain Lower-extremity sensory deficits Lower-extremity motor deficits that do not follow a dermatomal pattern Muscle atrophy Scoliosis Increased lumbosacral lordosis Sexual dysfunction Bladder and bowel dysfunction or incontinence Deformities of the lower extremities including pes cavus, pes equines, hammer toes, and leg-length discrepancies

168

n

Gait abnormalities Pain Cutaneous stigmata include hypertrichosis, a dermal pit, or a subcutaneous lipoma

Natural History n

n

Symptoms frequently progress slowly although there may be rapid post-traumatic progression. Primarily lower-extremity motor deterioration occurs over years. Symptoms exacerbated with prolonged bending or sitting

Diagnosis Differential diagnosis Disc disease n Peripheral neuropathy n Spinal cord tumors n Spondylolisthesis n Syringomyelia n

History Lower-extremity sensorimotor changes n Bowel or bladder dysfunction n

Exam Decreased motor function n Loss of cutaneous sensation n Spasticity n

Testing n MRI may note a thickened filum terminale (>2 mm diameter), mass, fibroadipose filum terminate, elongated spinal cord, and subarachnoid space obliteration. n Urodynamics n Electrodiagnostic studies, including pelvic floor studies n Somatosensory-evoked potentials Pitfalls Incorrect diagnosis of failed back syndrome or degenerative disc disease n The symptoms may be gradual, so that patients never seek medical care. n

Red Flags n

Sudden post-traumatic progression

Tethered Cord Syndrome

169

Injection n None Surgical n Surgical treatment is considered for new or worsening symptoms. n Preoperative percutaneous endoscopy n Patients are kept prone postoperatively for 2 to 5 days and are only allowed to walk if there is no CSF leak demonstrated on CT imaging. Consults Neurologic surgery n Physical medicine and rehabilitation Complications of treatment n Complications related to surgery include hemorrhage, CSF leak, headache, postoperative wound infection, pseudomeningocele Sagittal cervical T2-weighted magnetic resonance image following a remote C6–C7 spinal cord injury with heterogeneous T2 signal surrounding the spinal cord suggestive of scar tissue and cord tethering. (Adapted from Reis AJ. New surgical approach for late complications from spinal cord injury. BMC Surgery. 2006;6:12.)

Prognosis n

n n

Clinical improvement outcomes for pain, sensorimotor dysfunction, and bowel and bladder dysfunction range from 10% to 100%. Recovery of bladder function may occur with a short duration of symptoms Possible need for repeat detethering surgery in 3% to 16% of cases from several small studies

Treatment Medical n Supportive treatments may include medications for neuropathic pain and spasticity

Helpful Hints n

Detethering surgery or myelomeningocele repair in children results in extensive arachnoidal adhesions, causing variable adult outcomes.

n

Exercises Strengthening exercises

Suggested Reading


Kabayel DD, Ozdemir F, Unlu E, Bilgili N, Murat S. The effects of medical treatment and rehabilitation in a patient with adult tethered cord syndrome in the late postoperative period. Med Sci Monit. 2007;13(12):CS141–CS144.


n

Transverse Myelitis Description Transverse myelitis is an inflammatory process that affects the spinal cord.

n

Natural History n

Etiology/Types n n

Most commonly idiopathic Associated with connective tissue diseases and central nervous system infections

n n n n

Epidemiology n n

All age groups can be affected, with peaks at ages 10 to 19 years and 30 to 39 years. 1,400 new cases are diagnosed per year in the United States.

Pathogenesis n

n n n n

Possible postinfectious autoimmune process due to similar epitopes between the infectious agent and spinal cord antigen (eg, tuberculosis, coxsackie virus, hepatitis B vaccination) May also be caused by lymphocytic activation by microbial superantigens Perivascular monocytic and lymphocytic infiltration Demyelination is prominent in the white matter tracts. Axonal injury


Behçet’s disease Herpes virus HIV/human T-cell leukemia/lymphoma virus-1 Lyme disease Often follows respiratory, gastrointestinal, or systemic illness Sarcoidosis Sjogren’s syndrome Syphilis Systemic lupus erythematosus 30% of pediatric cases have a history of immunization within the past month.


Motor, sensory, and autonomic dysfunction Can be a presenting feature of multiple sclerosis Rapidly progressive paralysis over minutes, hours, or days Pain located at the back, abdomen, and extremities.

170

Bowel and bladder dysfunction

n n

Rapidly progressive paralysis over minutes, hours, or days About 50% of patients become paraplegic Bowel and bladder dysfunction Numbness Paresthesias/dysesthesias Symptoms usually stop progressing after about 2 to 3 weeks. Persistent severe disability

Diagnosis Differential diagnosis Arteriovenous malformation n Guillain-Barré syndrome n Ischemia n Multiple sclerosis n Vasculitis n Viral myelitis n

History Determine time course and extent of neurologic deficits n Assess for prior history of recent infection, vaccination, trauma, systemic inflammatory disease, ischemia, radiation exposure, neoplasm, or multiple sclerosis n Bowel, bladder, and sexual dysfunction n

Exam Assess motor, sensory, reflex changes n Assess level of spinal cord injury n

Testing Diagnosis is confirmed by CSF pleocytosis, elevated CSF IgG index, or enhancement of the spinal cord with contrast-enhanced MRI. n MRI usually notes increased T2-weighted signal within the spinal cord and about 74% of patients demonstrate contrast enhancement. n

Pitfalls MRI may be negative in up to 40% of cases.

n

Red Flags n n

Rapidly progressive neurologic changes Bowel or bladder dysfunction

Transverse Myelitis n n n

171

Stretching to prevent soft tissue contractures during the acute phase Strengthening program Aerobic conditioning

Modalities n None Injection n None

Consults n Physical medicine and rehabilitation n Neurology Complications of treatment n Variable, based on the severity of the neurologic deficits Sagittal thoracic T2-weighted magnetic resonance image demonstrating increased spinal cord signal spanning several levels (arrow) consistent with acute transverse myelitis. (Adapted from Fast A, Goldsher D. Navigating the Adult Spine: Bridging Clinical Practice and Neuroradiology. New York: Demos Medical Publishing, 2007:70.)

Prognosis n

n n n

Treatment Medical A 5-day course of intravenous methylprednisolone 1,000 mg per day followed by an oral steroid taper may improve motor recovery. n Plasma exchange may be considered in patients who do not respond to intravenous steroids. n Intravenous cyclophosphamide n Bowel and bladder retraining n Sexual dysfunction training n

Exercises n Occupational therapy for activities of daily living

n

One-third of patients recover completely, one-third have permanent moderate disability, one-third have severe disability. Recurrent disease may occur. Most patients recover neurologically within 6 months but recovery can continue for 2 years. Poor outcome is associated with back pain, rapid progression of symptoms, cervical sensory changes, and spinal shock. Interleukin-6 in the CSF strongly correlates with eventual disability.

Helpful Hints n

Depression often accompanies transverse myelitis.

Suggested Reading Krishnan C, Kaplin AI, Pardo CA, Kerr DA, Keswani SC. Demyelinating disorders: update on transverse myelitis. Curr Neurol Neurosci Rep. 2006;6(3):236–243.


Surgical n None

Whiplash-Associated Disorders Description Whiplash-associated disorders are caused by forceful acceleration-deceleration forces in the neck resulting from rear-end or side impact, most commonly due to motor vehicle accidents.

n

Temporomandibular dysfunction is related to forceful rapid jaw opening with neck extension stretching the capsule and disrupting the disc.

Risk Factors n

Spondylosis

Etiology/Types n

Quebec Task Force Classification – Grade 1: neck complaints including pain, stiffness, or tenderness, without physical signs – Grade 2: neck complaints and musculoskeletal signs including point tenderness and decreased cervical range of motion – Grade 3: neck complaints and neurologic signs including upper-extremity paresthesias, muscle fatigue, a sense of heaviness – Grade 4: neck complaints with fracture or dislocation

Clinical Features n n n n n n n n n

Epidemiology n n n

Based on insurance claims, the incidence ranges from 0.1% to 14.5% per 1,000 population Affects 20% to 83% of patients involved in motor vehicle collisions Common cause of chronic disability

Pathogenesis n n n

n

n n n

Controversial Generally thought to be related to cervical sprain or strain Forward acceleration of the trunk and shoulders during a rear-end collision causes the cervical spine to assume an S-shaped curve with the upper cervical spine in flexion and the lower cervical spine in extension followed by neck flexion. Can result in tears of the ligamentum flavum, anterior longitudinal ligament, and capsular ligaments; disruption of the annulus of the intervertebral disc; fractures of the zygapophyseal (facet) joints, articular pillar, endplates, and vertebral bodies. Muscles do no have time to react to the sudden force. Strain or tear of the sternocleidomastoid, scalene, or longus colli muscles Longus colli muscle tears may also cause injury to the sympathetic trunk, resulting in Horner’s syndrome, dizziness, and nausea.

172

n n

Primarily a clinical diagnosis Delayed onset of symptoms up to 12 to 14 hours later, following the inciting event Neck pain at rest or with movement Neck stiffness Headache is the second most common symptom. Upper-extremity pain and paresthesias Jaw pain Visual changes caused by increased sympathetic tone Dizziness due to vestibular dysfunction or injury Memory and concentration dysfunction Psychological distress

Natural History n

Pain generally resolve within 12 weeks, although up to 39.6% of patients may have pain for as long as 7 years.

Diagnosis Differential diagnosis Cervical fracture or dislocation or both n Cervical radiculopathy n Occipital neuralgia n

History Delayed onset of symptoms, up to 12 to 14 hours following the inciting event n Neck pain at rest or with movement n Neck stiffness n Headache is the second most common symptom. n

Exam Decreased cervical range of motion in all planes, mostly affecting flexion and extension

n

Testing n Imaging can be used to rule out fractures and ligament or disc injuries. n Lateral flexion–extension X-rays may demonstrate loss of the normal lordosis and kyphotic angle, which

Whiplash-Associated Disorders

Pitfalls Clinical diagnosis based on symptoms and mechanism of injury

n

Red Flags n

Cervical fracture or dislocation or both

Treatment Medical n Early mobilization may improve outcome. n Immobilization and rest are not recommended. n NSAIDs n Muscle relaxants n Mild analgesics n Intravenous methylprednisolone n Driving should be avoided during the acute stage.

Surgical n Considered in the treatment of fracture or dislocation or both Consults Physical medicine and rehabilitation n Neurologic and orthopedic-spine surgery n

Complications of treatment n Persistent disabling pain n Disability

Prognosis n n n n n n

Exercises Cervical range of motion exercises

n

Modalities n Heat, cold, ultrasound, and transcutaneous electrical nerve stimulation have been used for symptomatic relief of pain and muscle spasms. n Traction Injection Medial branch blocks and percutaneous radiofrequency neurotomy of the medial branches of C2–C3 or below have been found to be helpful for up to 1 year.

n

n

Pain generally resolve within 12 weeks. 50% of adults report neck pain 1 year following the injury. 39.6% of patients may have pain as long as seven years. Slower recovery in patients with greater symptom severity Poor recovery related to postinjury psychological distress, passive coping strategies Prolonged worker’s compensation found to be related to the severity of the collision, lack of seat belt use, nonrear-end impact, riding in a vehicle other than a car or taxi, female gender, older age, and number of dependents 14% to 42% of patients will develop chronic neck pain.

Helpful Hints n n

Important to rule out fracture Attempt to search for a possible specific diagnosis while treating the associated disorders

Suggested Reading Rodriquez AA, Barr KP, Burns SP. Whiplash: pathophysiology, diagnosis, treatment, and prognosis. Muscle Nerve. 2004;29(6):768–781.


is thought to be due to a hypermobile segment adjacent to a hypomobile segment that results from muscle spasm.

173

Zygapophyseal (Facet) Joint Pain, Cervical Description

Natural History

Cervical zygapophyseal (facet) joint pain is due to a noninflammatory degenerative joint disease that is characterized by progressive joint stiffness, decreased range of motion, and pain.

n


Multifactorial type includes genetic, biochemical, and biomechanical factors Traumatic type includes fracture, dislocation, and whiplash injuries. Degenerative type includes osteoarthritis.

Epidemiology n n n

X-ray findings are nearly universal in individuals aged 65 years and older. Severity increases with advancing age. Prevalence estimates range from 25% to 63%.

Pathogenesis n

n n n

n

Zygapophyseal (facet) joints are diarthrodial joints that are made of a fibrous capsule lined with a synovial membrane containing articular cartilage and menisci. C0–C1 and C1–C2 are innervated by cervical ventral rami. C2–C3 is innervated by two different branches of the C3 dorsal ramus. C3–C4 to C8–T1 are innervated by the medial branches of the cervical dorsal rami, above and below the joint. Not exclusively a disorder of articular cartilage but includes periarticular bone, synovial lining, and adjacent connective tissue.


Heredity Increasing age, although not universal Joint instability or malalignment Neck hyperextension injury Trauma

Unknown

Diagnosis Differential diagnosis n Cervical discogenic pain n Cervical spinal stenosis n Fibromyalgia n Muscle strain or sprain n Myofascial pain syndrome n Neuralgic amyotrophy n Occipital neuralgia n Shoulder pathology n Spinal cord injury n Syringomyelia n Thoracic outlet syndrome History Axial neck pain with radiation from the suboccipital region to the shoulders or midback

n

Exam There are no physical examination findings that are specific for zygapophyseal (facet) joint pain. n Possibly worsens with neck motion in a certain plane n Decreased neck range of motion n

Testing X-rays are useful to screen for instability, fractures, and osteoarthritis n Flexion–extension X-rays are used to assess for instability. n MRI has demonstrated degenerative joints in up to 75% of asymptomatic adults in the seventh decade of life. n SPECT may be useful. n Small fractures may be present that are not detected with advanced imaging. n

Pitfalls Results of imaging need to be correlated with the patient’s presenting history and physical examination.

n


Axial neck pain with radiation from the suboccipital region to the shoulders or midback There are no history or physical examination findings that are specific for zygapophyseal (facet) joint pain.

174

Red Flags n

Neurologic dysfunction

Zygapophyseal (Facet) Joint Pain, Cervical

Medical n NSAIDs n Analgesics Exercises Cervical range of motion n Traction n

Modalities Heat, cold, ultrasound, and transcutaneous electrical nerve stimulation have been used for symptomatic relief of pain and muscle spasms. n Spinal manipulation and mobilization n

Injection n Fluoroscopically guided cervical zygapophyseal (facet) intra-articular block or medial branch block n Radiofrequency neurotomy of the medial branches of the dorsal rami has been shown to decrease pain from several months to 1 year. n Pulsed radiofrequency of the medial branches of the dorsal rami has demonstrated improvement up to 4 months in several small studies.

Surgical n Cervical fusion Consults n Physical medicine and rehabilitation n Neurologic or orthopedic-spine surgery Complications of treatment n Complications related to interventional procedures n Complications related to surgery

Prognosis n

Unknown

Helpful Hints n

n

There are no history or physical examination findings that are specific for zygapophyseal (facet) joint pain. Results of imaging need to be correlated with the presenting history and physical examination.

Suggested Reading Kirpalani D, Mitra R. Cervical facet joint dysfunction: a review. Arch Phys Med Rehabil. 2008;89(4):770–774.


Treatment

175

Zygapophyseal (Facet) Joint Pain, Lumbar Description

Clinical Features

Zygapophyseal (facet) joint pain is due to a noninflammatory degenerative joint disease that is characterized by progressive joint stiffness, decreased range of motion, and pain resulting in loss of mobility.

n

Etiology/Types

n

n n n n

Multifactorial etiology Genetic factors Biochemical factors Repetitive strain and low-grade trauma

n n

n

n

Epidemiology n n

n n n

Most common at the L5–S1 level followed by the L4–L5 and L3–L4 levels Prevalence of zygapophyseal (facet) joint pain ranges from 15% in the younger population to 54% in the elderly population. Zygapophyseal (facet) joint arthrosis usually begins in the third decade of life. Radiographic findings are nearly universal in individuals aged 65 years and older. More common in males compared with females

Pathogenesis n

n n n

n n

Not exclusively a disorder of articular cartilage but also includes periarticular bone, synovial lining, adjacent connective tissue. Can be associated with disc degeneration 16% of the axial compressive force passes through the joints with standing and 0% occurs with sitting. With increased intervertebral disc herniation there is an increased axial loading of the zygapophyseal (facet) joints. Several studies demonstrate correlation between tropism and degenerative disc disease. Capsular irritation can result in reflexive spasm of the erector spinae and multifidus muscles.

Risk Factors Heredity Increasing age, although not universal n Intervertebral disc degeneration n Muscle weakness n Peripheral neuropathy n Recurrent rotational strains n Three-joint unit instability or malalignment 176 n n

Symptoms range from asymptomatic to severe pain in the lower back and legs with difficulty walking. Morning stiffness Pain exacerbated with lumbar extension and/or ipsilateral rotation or descending stairs. Pain improved with flexion Postural changes include age-related loss of lumbar lordosis that offloads the degenerative zygapophyseal (facet) joints. Referred pain associated with lower lumbar zygapophyseal (facet) joints usually extends into the lower lateral leg and occasionally to the foot.

Natural History n n

Increased risk of joint changes and pain with increasing age, although not universal Back pain is less common in former athletes compared with controls even in the presence of spondylosis.

Diagnosis Differential diagnosis n Acute or chronic infection n Ankylosing spondylitis n Degenerative disc disease n Reactive arthritis n Rheumatoid arthritis n Trauma History Research has not demonstrated a reliable clinical feature that correlates with zygapophyseal (facet) joint pain. n Dull aching pain n Pain generally thought to improve with flexion and worsen with extension and/or rotation, or with descending stairs. n

Exam n Generally believed that pain is exacerbated with lumbar extension and/or ipsilateral rotation. n Lumbar paraspinal tenderness may be present, particularly in the sacral sulcus. Testing Lumbar X-rays may demonstrate loss of disc height and zygapophyseal (facet) joint sclerosis and degeneration.

n

Zygapophyseal (Facet) Joint Pain, Lumbar n n

177

Analgesics Transdermal anesthetic and anti-inflammatory patches in the older population

Exercises General strengthening and stretching exercises n Yoga n

Injection n Fluoroscopically guided radiofrequency denervation of the medial branches of the target zygapophyseal (facet) joint n Fluoroscopically guided intra-articular joint steroid and local anesthetic injections Axial lumbar T2-weighted magnetic resonance image demonstrating increased signal within the zygapophyseal joints (arrows) suggestive of an inflammatory reaction.

n n

n

Bone scan demonstrates increased uptake in regions of joint subchondral sclerosis. MRI may demonstrate thickened, irregular zygapophyseal (facet) joints with increased T2-weighted fluid signal within the joint space. Fluoroscopically guided anesthetic blockade of the suspected zygapophyseal (facet) joint or the corresponding medial branches is the most reliable test for identifying the specific zygapophyseal (facet) associated with the pain, but the false positive rate ranges from 25% to 41%.

Pitfalls A distended joint capsule may compress a nerve root or the spinal cord. n Considerable overlap of pain referral patterns n

Red Flags n

Progressive neurologic dysfunction

Surgical Lumbar fusion

n

Consults n Physical medicine and rehabilitation n Neurologic or orthopedic-spine surgery Complications of treatment n Complications related to surgery include infection and bleeding, general anesthesia risks. n Complications related to the interventional procedures include neuritis in up to 5% of patients.

Prognosis n

n

Radiofrequency denervation has been shown to provide up to 1 year of relief with anecdotal reports of longer duration in select patients Surgery has been shown to result in improvement in select patients.

Helpful Hints n

Beware of considerable overlap of pain referral patterns.

Treatment

Suggested Reading

Medical n NSAIDs

Cohen SP, Raja SN. Pathogenesis, diagnosis, and treatment of lumbar zygapophyseal (facet) joint pain. Anesthesiology. 2007;106(3):591–614.


Modalities n Heat, cold, ultrasound, and transcutaneous electrical nerve stimulation have been used for symptomatic relief of pain and muscle spasms. n Spinal manipulation and mobilization


II

Spine-Mimicking Conditions

Carpal Tunnel Syndrome Description

n

Carpal tunnel syndrome caused by compression of the median nerve within the carpal tunnel is the most common focal compression neuropathy of the upper extremity.

n

Etiology/Types n

Compression of the median nerve as it passes through the carpal tunnel, due to swelling of the flexor tendon lining, fracture, joint dislocation, or inflammatory arthritis

Epidemiology n n n

Lifetime risk of 10% Female to male ratio 3:1 Neck pain in those with median nerve sensory abnormalities is 24%.

Pathogenesis n

Compression of the median nerve due to a variety of factors results in loss of motor and sensory function along the distribution of the median nerve in the hand.

Risk Factors n n n n n n n n n n n n

Amyloidosis Awkward wrist positioning Diabetes Edema Gout or pseudogout Hypo- or hyperthyroidism Lyme disease Most cases not work related Obesity Pregnancy Repetitive hand motions Septic arthritis


Numbness or paresthesias of the palmar side of the radial three and one-half digits Thenar atrophy with severe disease Loss of dexterity Inability to pick up or manipulate small objects Dull aching discomfort in the forearm or upper arm may occur in up to 45% of patients and is associated with milder median nerve entrapment at the wrist and greater hand paresthesias.

180

84% of confirmed cases have nocturnal hand paresthesias. 82% have paresthesias aggravated by activities of the hand.

Natural History n

n n

n

Progressive pain followed by increasing numbness, tingling and/or weakness of the median nerve innervated sensory, and motor distribution Pain eventually subsides as neurologic deficits worsen. Wasting of the thenar muscles results in a “simian hand” and loss of the ability to oppose the thumb to the little finger. Loss of manual dexterity with disease progression

Diagnosis Differential diagnosis Anterior interosseous nerve syndrome n C6 or C7 radiculopathy n Pronator syndrome n Supracondylar process syndrome n

History Numbness or paresthesias of the palmar side of the radial three and one-half digits, hand, and wrist n Pain may radiate distally into the hand or proximally up the arm. n Progressive tingling during the day n Pain worse in the evening n “Flick” sign is often described by patients who “flick” their wrist to relieve symptoms. n

Exam Tinel’s test is positive if tingling is reproduced with tapping of the median nerve at the wrist from proximal to distal; 87% specificity. n Phalen’s test or the reverse Phalen’s test reproduces a patient’s pain with wrist flexion or extension to 90 degrees, respectively at 60 seconds; 60% specificity. n Durkin’s compression test is positive if symptoms are reproduced with direct compression of the carpal tunnel. n Weak thumb abduction is rare. n Thenar atrophy is rare. n Loss of sensation over the median distribution n

Carpal Tunnel Syndrome

Pitfalls Pregnancy-related symptoms usually resolve following delivery.

n

Red Flags n n

Severe weakness or numbness “Simian hand”

Treatment Medical Education to avoid repetitive wrist and hand movements n Wrist splints at a neutral angle are most effective when used within 3 months of symptom onset. n Wrist splints only at night are not as effective as fulltime use. n Short-term NSAIDs n Oral prednisone may be helpful in the short term. n

Injection n Steroid injection into the carpal tunnel may provide temporary relief. Surgical Open or endoscopic surgical release of the transverse carpal tunnel ligament is considered in patients with severe nerve entrapment who have not responded to conservative treatment.

n

Consults Physical medicine and rehabilitation n Orthopedic hand surgery n Plastic surgery n

Complications of treatment n Surgical complications include nerve or arterial injury, hypertrophic scarring, tendon damage, stiffness, postoperative infection, hematoma

Prognosis n n

Symptoms recur in about 80% of patients after 1 year with conservative treatment. A 2-year follow up of untreated carpal tunnel syndrome noted that 67% of patients remained the same electrodiagnostically with almost 8% deteriorating and 25% improving.

Helpful Hints n

Carpal tunnel syndrome is a clinical diagnosis with electrodiagnostic confirmation.

Exercises Nerve and tendon gliding exercises n Strengthening and stretching

Suggested Reading

Modalities n Ultrasound

Chow CS, Hung LK, Chiu CP, et al. Is symptomatology useful in distinguishing between carpal tunnel syndrome and cervical spondylosis? Hand Surg. 2005;10(1):1–5.

n

Section II: Spine-Mimicking Conditions

Testing Electrodiagnostic testing is used to diagnose, assess severity, and to rule out cervical radiculopathy, plexopathy, and peripheral neuropathy. n Normal electrodiagnostic studies may be found in up to 8% of patients with symptoms. n MRI is used to assess for cysts, tenosynovitis, and aberrant muscles. n

181

Complex Regional Pain Syndrome (Reflex Sympathetic Dystrophy) Description

Pathogenesis

Complex regional pain syndrome is a chronic pain syndrome that often develops with or without an inciting event, is more severe than the original injury, and leads to pain and functional loss of the affected extremity and eventual impairment.

n

Etiology/Types

n

Thought to be caused by the sympathetic nervous system or an immune response n 14% to 46% report a minor fracture. n 10% to 29% report a sprain or strain. n 3% to 24% occurs postsurgery. n 2% to 25% report no inciting event. n Reported in up to 61% of poststroke patients n International Association for the Study of Pain (IASP) classification type 1 reflex sympathetic dystrophy (RSD) – Syndrome that develops following a noxious event, the severity or which is disproportionate to the inciting event. – No nerve lesion – Symptoms may not be isolated to the affected nerve distribution. – The affected area may demonstrate changes in cutaneous blood flow, sudomotor activity, edema, and hyperalgesia or allodynia. – More common than type 2. – Often mild presentation n IASP classification of type 2 – Causalgia, allodynia or hyperpathia after major trauma and/or major nerve injury – May not be isolated to the affected nerve distribution – The affected area may demonstrate changes in cutaneous blood flow, sudomotor activity, edema, and hyperalgesia or allodynia. – Often affects the hand or foot. – Often severe presentation

n

n n

Sensitization of primary nociceptor afferents results in the release of inflammatory mediators Sensitization of the sympathetic nervous system Pseudoinflammatory

Risk Factors n

n n n

Clinical Features n n n n n n n n n n n n n n

Incidence is greater than 26 per 100,000. Most common in older women with an upper limb fracture n Mean age range from 36 to 46 years n Female predominance 182

Erythematous or cyanosed blotchy skin Skin atrophy Skin edema occurs in up to 81% of patients Loss of normal skin creases Reduced or excessive sweating Increased or decreased temperature Excess or loss of hair Nail ridges, clubbing, curve, or brittleness Restricted passive range of motion, contractures Osteoporosis Muscle wasting and weakness with up to 78% reporting greatly decreased grip strength Myoclonic jerks, spasms, dystonia, tremor Urinary sphincter or detruser dysfunction Allodynia—normal sensory stimuli causing pain

Natural History n

n

Epidemiology n

Immobilization Increased risk with human leukocyte antigen-DQ1, DR13, and DR2 Limb trauma such as ankle sprain, scaphoid fracture, crush injury, or following surgery Type 2 is more common with brachial plexus avulsions. Psychological predisposition

n

n

n

Stage 1: early acute stage characterized by pain and sensory dysfunction, vasomotor and sudomotor dysfunction, and edema Stage 2 (dystrophic stage): occurs within 3–6 months and is characterized by increased pain and sensory and vasomotor dysfunction, as well as motor and trophic changes Stage 3 (atrophic stage): characterized by decreased pain and sensory dysfunction with continued vasomotor dysfunction with increased motor and trophic changes Loss of limb function

Complex Regional Pain Syndrome

Differential diagnosis n Fracture n Neuropathy/neuropathic pain n Radiculopathy History n Usually spontaneous and severe burning pain n Variable weakness or muscle wasting n Involuntary movements n Predominately in the distal extremity n Hypo- or hyperalgesia and allodynia Exam 74% of patients present with allodynia. n 70% report decreased joint range of motion. n 66% report skin color asymmetry. n 56% report skin temperature asymmetry. n 56% report weakness. n 14% report dystonia. n 9% report tremor. n

Testing Is used to rule out other disorders n X-rays may demonstrate spotty osteoporotic changes in the affected limb. n Bone scan may demonstrate increased uptake indicating increased bone metabolism. n Electrodiagnostic studies can be used to rule out neurologic causes. n

Pitfalls n Unpredictable course

Red Flags n n

Loss of limb function Severe pain

Treatment Medical Immobilization for as short a time as possible.

n

n n n

Trial of gabapentin, tricyclic antidepressants, duloxetine, opioids, bisphosphonates, prednisone, vitamin C Psychological evaluation in patients with two or more months of symptoms Remove aggravating factors

Exercises n Joint range of motion n Stress loading of the limb n Coordination/dexterity n Aquatic therapy Modalities n Compression devices for edema management n Contrast bath for desensitization n Transcutaneous electrical nerve stimulation Injection n Sympathetic block n Intravenous regional block Surgical n Intrathecal baclofen n Spinal cord stimulator Consults n Pain management Complications of treatment n Variable

Prognosis n n n

May resolve within weeks or continue for years Only 29% of patients become pain free. Severe impairments in up to 64% of patients

Helpful Hints n n

Important to identify and treat earlier in the course of the disease Surgery may worsen symptoms.

Suggested Reading Atkins RM. Complex regional pain syndrome. J Bone Joint Surg Br. 2003;85(8):1100–1106.


Diagnosis

183

Fibromyalgia Description Fibromyalgia is an idiopathic, chronic, nonarticular, soft tissue pain syndrome with widespread musculoskeletal pain and generalized tender points.

Etiology/Types n n

Unknown genetic and environmental factors Possible role for polymorphisms of genes in the serotoninergic, dopaminergic, and catecholaminergic systems

Epidemiology Underdiagnosed Prevalence is reported to be 3.4% in females and 0.5% in males. n Most commonly affects women 20 to 50 years of age. – Also described in males, adolescents, and children n n

original criteria was formed as part of a research protocol. – Bilateral widespread pain above and below the waist including the axial spine for at least 3 months – Presence of 11 tender points among the nine pairs of specified sites (18 points). Using moderate and consistent pressure of the dominant thumb [8.8 lbs (4.0 kg)], which should begin to blanch the examiner’s thumbnail n Sleep disturbance n Cognitive difficulties n Fatigue n Headache n Morning stiffness n Paresthesias n Anxiety

Natural History n

Pathogenesis n

n

Part of a spectrum of diseases called central sensitization syndromes, characterized by systemic symptoms including muscle pain Other central sensitization syndromes commonly associated with fibromyalgia include irritable bowel syndrome, irritable bladder, dysmenorrhea, premenstrual syndrome, restless leg syndrome, and temporomandibular joint pain


Anxiety Depression Epstein–Barr virus Lyme disease Parvovirus Peripheral pain syndrome Physical trauma Predisposing social characteristics include divorce, failure to complete high school, and low income. Q fever Somatization disorder

Clinical Features n

Diagnosis is based on the American College of Rheumatology 1990 criteria, although a number of physicians have been critical of its usefulness as the

184

Progressive pain occasionally associated with disability

Diagnosis Differential diagnosis Chronic fatigue syndrome n Conversion disorder n Hypothyroidism n Metabolic or inflammatory myopathies n Myofascial pain syndrome n Polymyalgia rheumatica n

History n Pain at multiple sites n Low back pain n Neck pain n Stiffness, burning, or soreness that improves throughout the day n Subjective swollen joints or paresthesias without objective findings n Worsened by cold or humid weather, poor sleep, and physical or mental stress n Improved with warm and dry weather, moderate physical activity, relaxation, and proper sleep Exam Decreased activity may manifest as weakness on motor testing and decreased coordination and endurance

n

Fibromyalgia

Pitfalls Should not be a diagnosis of exclusion

n

Red Flags n

Severe pain

Treatment Medical Antidepressant medications such as amitriptyline or selective serotonin reuptake inhibitors n Ultram n Cyclobenzaprine n Pregabalin n NSAIDs n Analgesics n Cognitive behavioral therapy is used to help patients understand the effect of thoughts, expectations, and beliefs on symptoms. n Patient education through lectures, handouts, or group meetings n Proper sleep hygiene n

Exercises n General strengthening, stretching, and conditioning program n The type of exercise is not important as much as maintaining the exercise regimen. n Improvement may be related to endogenous opioid production or by increasing resistance to microtrauma related to daily activity.

Modalities n Heat, cold, ultrasound, and transcutaneous electrical nerve stimulation have been used for symptomatic relief of pain and muscle spasms. Injection Trigger point injections for symptoms of myofascial pain

n

Surgical None

n

Consults n Rheumatology n Physical medicine and rehabilitation n Psychiatry or psychology to address anxiety, depression, and kinesiophobia n Vocational rehabilitation Complications of treatment n Variable

Prognosis n

Currently there is no treatment but patients may be able to lead normal functional lives with treatment.

Helpful Hints n

Important to address the psychological impact of the disease as well as the physical impact

Suggested Readings Clauw DJ. Fibromyalgia: update on mechanisms and management. J Clin Rheumatol. 2007;13(2):102–109. Harden RN. Muscle pain syndromes. Am J Phys Med Rehabil. 2007;86(suppl l):S47–S58.


Testing Used to rule out other diagnoses

n

185

Herpes Zoster Description Herpes zoster, also known as shingles, is a latent reactivation of varicella-zoster infection (chicken pox) characterized by an erythematous, papular, and/or vesicular rash that is associated with pain in the distribution of a peripheral sensory nerve root.

n n

Natural History n

Etiology/Types n

Caused by the varicella-zoster virus (VZV), which is one of the eight herpes viruses

n n

Epidemiology n

More common in the elderly and in individuals with decreased immune function


n n

n n

VZV attaches to the hosts cells by binding to a heparin sulfate proteoglycan. The initial infection, known as chicken pox, is associated with a viremia and cutaneous eruptions. The VZV remains dormant in the sensory ganglion of the spinal cord. The virus reactivates with decreased host immunity, spreading within the cutaneous sensory neuron found within the dorsal root ganglion, and traveling centrally and peripherally within the nerve. Large, myelinated sensory fibers are most commonly affected. Inflammation and hemorrhage within the dorsal root ganglion, the posterior horn of the spinal cord. and corresponding motor neuron on the anterior horn VZV reactivation also scars and fibrosis the peripheral nerve. Patient is infectious during the reactivation period and prior to the development of vesicles.

Risk Factors n n

Advancing age Decreased immune activity


4- to 28-day prodome of nonspecific constitutional symptoms such as fever and malaise Pain first develops 4 to 7 days before the skin manifestations. Cutaneous erythema, edema, vesicular eruptions, and hemorrhage eventually develop.

186

Scarring, atrophy, and macular or papular depigmentation 55% of cases affect the thoracic spinal nerves.

n

n n n

Pain along a dermatome begins first, followed a week later by erythematous skin papules that coalesce into vesicles. The vesicles dry within days Immunosupressed individuals may develop transverse myelitis, encephalitis. or cerebral vasculitis with associated signs and symptoms. Postherpetic neuralgia occurs with continued pain following the resolution of cutaneous disease and may take 2 to 4 weeks to resolve. Persistent postherpetic neuralgia is reported by up to 50% of patents aged 70 years and above. Depression may occur due to the persistent pain. Visceral or autonomic nerve dysfunction

Diagnosis Differential diagnosis Herpes simplex virus n Intercostal neuralgia n Muscle strain n Radiculopathy n Superficial pyoderma n

History Shooting, burning, tingling, or sharp pain with skin dysesthesias along the sensory nerve distribution n Localized erythematous papules develop within a week, which form into vesicles following a segmental distribution, but may include up to three dermatomes. n

Exam Skin lesions begin as an erythematous region and eventually coalesce into vesicles and groups of vesicles on an erythematous base. n Cutaneous lesions do not cross the midline. n The vesicles crust and desquamate within 3 weeks. n Old lesions appear as hypopigmented macules or papules. n Motor loss, which is usually temporary, may be associated with corresponding motor neuron involvement. n Fever and localized lymphadenopathy n

Herpes Zoster

187

n

Testing Viral culture n Direct immunofluorescence assay

Injection n Postherpetic neuralgia may be treated with local nerve root blocks.

Pitfalls Dysesthetia or total sensory loss at the site of involvement

n

Red Flags n

The patient may be contagious if seen prior to the development of dry crusted vesicles.

Treatment Medical Patients with vesicles should have limited exposure to other people. n Healthy patients younger than 50 years of age can be treated with analgesics, antipruritics, mild sedatives, topical antibiotic ointment. n Immune-competent patients aged 50 years and older can be treated with corticosteroids, valacyclovir, or adenosine monophosphate. n Immunocompromised patients should be treated with aggressive antiviral therapy. n Postherpetic neuralgia can be treated with amitriptyline, gabapentin, topical capsaicin, or lidocaine patch. n

Surgical None

Consults n Infectious disease n Dermatology if the presenting signs and symptoms are atypical n Physical medicine and rehabilitation Complications of treatment n Variable

Prognosis n n n

Usually self-limiting Most commonly results in no or minimal disability Older patients are more likely to demonstrate postherpetic neuralgia, which may result in significant disability.

Helpful Hints n n

Not associated with lumbar radiculopathies Patients are infectious prior to the development of vesicles.

n

Exercises None

Suggested Reading

Modalities n Postherpetic neuralgia may be treated with a transcutaneous electrical nerve stimulator.

Straus SE, Ostrove JM, Inchauspé G, et al. NIH conference. Varicella-zoster virus infections. Biology, natural history, treatment, and prevention. Ann Intern Med. 1988;108(2):221–237.


n

Hip–Spine Syndrome Description

Clinical Features

Hip–spine syndrome (HSS) describes a symptom complex resulting from concurrent degenerative hip and degenerative disc disease of the lumbar spine.

n

n

Etiology/Types n n

n n

Degenerative changes in the hip and lumbar spine increase with advancing age. Simple HSS: Pathology from either the hip or the spine that is clearly identified as the primary cause of pain. Complex HSS: Degenerative changes at the hip and spine that both contribute to the pain complaint. Secondary HSS: Hip and spine pathology that are interrelated due to a hip flexion, adduction deformity of the hip, or scoliosis.

Epidemiology n

n

Radiographic changes associated with hip osteoarthritis are found in up to 12% of patients older than 80 years of age. MRI findings of spinal stenosis are found in up to 20% of asymptomatic patients over 60 years of age.

Pathogenesis n

n n n

n

n

L4 nerve root involvement can present with weakness and wasting of the quadriceps muscles and loss of the patellar reflex. Synovitis of the hip may result in buttock pain that radiates to the groin and down the anterior thigh. A fixed flexion deformity may result with continued inflammation at the hip joint. A flexion deformity of the hip may rotate the pelvis forward, increasing the lumbar lordosis and resulting in increased zygapophyseal (facet) joint subluxation and foraminal narrowing. Scoliosis may cause pelvic tilt uncovering the ball of the femur on the socket, increasing the risk for hip joint degeneration. A fixed hip adduction deformity may cause pelvic obliquity, resulting in lumbar scoliosis and eventually causing nerve root involvement.

Risk Factors n n n

Alterations at the L4–L5 and L5–S1 lumbar discs Poor posture and sagittal alignment Antalgic gait

188

Hip pain, L3–L4 segment instability or L4 root involvement can present as pain over the anterior aspect of the thigh. A limp, groin pain, and limited hip internal range of motion are more predictive of a hip disorder.

Natural History n

Progressive pain and mobility deficit

Diagnosis Differential diagnosis n Avascular necrosis of the hip n Greater trochanteric bursitis n Groin pain related to an L3 or L4 radiculopathy n Hip osteonecrosis n Labral tear n Sciatica History Groin pain is more common with true intra-articular hip pathology. – Pain is exacerbated by ambulation but relieved with rest. – Progression to continued pain at night n Buttock and back pain can be difficult to differentiate. n

Exam The goal is to isolate the hip joint and lower lumbar region while attempting to reproduce the characteristic pain. n A femoral nerve stretch with hip hyperextension while the patient is prone can reproduce the characteristic pain of an L4 radiculopathy. n Ely’s test involves having the patient prone, fully flexing the knee, pushing the heel toward the buttock. – Stretching of the rectus femoris will cause the hip to flex, causing the buttocks to rise. n There may be wasting of the quadriceps muscle. n Pain may be reproduced with hip flexion or internal rotation. n Limited internal hip range of motion n Antalgic gait n Often physical exam findings are difficult to differentiate from age-expected changes. n Straight leg raise to assess for radiculopathy n

Hip–Spine Syndrome

Testing n X-rays may demonstrate hip joint osteoarthritis. n MRI is useful in assessing hip joint pathology, labral tears, or fracture as well as axial spine pathology. n CT may be used to assess for joint pathology or fracture. Pitfalls Improper diagnosis

n

Red Flags n n n

Severe quadriceps muscle wasting Severe weakness, numbness, or tingling in the lower extremities Bowel or bladder changes

Treatment Medical NSAIDs and analgesics

n

Exercises Myofascial release of the hip flexor contracture n Pelvic alignment and stability n Lower-extremity strengthening and stretching

n

189

Fluoroscopically guided, contrast-enhanced L3 or L4 nerve root block is used to assess its contribution to hip pain.

Surgical A hip osteotomy or total hip arthroplasty may correct the hyperlordosis, possibly relieving lower back pain, although it has not been demonstrated to change spinal sagittal radiographic angles. n With severe spinal stenosis, lumbar decompression should be considered first. n

Consults Physical medicine and rehabilitation n Neurologic or orthopedic-spine surgery n

Complications of treatment n Lumbar decompression for patients with spine disorders will not alleviate the pain associated with a hip arthrosis. n Foot drop following hip arthroplasty can occur in patients with severe spinal stenosis; thought to be related to a double-crush nerve injury.

n

Injection Trigger point release of the iliopsoas muscle n Fluoroscopically guided or ultrasound-guided hip anesthetic block can be used assess hip joint involvement. n

n

Good for patients in whom the underlying pathology is identified.

Helpful Hints n

Always screen the hip and lumbar spine to help with possible differentiation in all patients with either complaint.

Suggested Reading Ben-Galim P, Ben-Galim T, Rand N, et al. Hip-spine syndrome: the effect of total hip replacement surgery on low back pain in severe osteoarthritis of the hip. Spine. 2007;32(19):2099–2102.



n

Prognosis

Lyme Disease Description

n

Lyme disease is a tick-borne infectious disease that can result in progressive rheumatologic, neurologic, and cardiac dysfunction. n

Etiology/Types n

n

Lyme disease is caused by the spirochete Borrelia burgdorferi. n

Epidemiology n n n

n

Most common vector-borne infectious disease in the United States 15,000 cases are reported annually. Most common in the Northeast and Midwest regions of the United States as well as the California and Oregon coasts. Endemic areas are associated with large deer populations, which carry the tick species Ixodes, responsible for transmitting B. burgdorferi to humans.

Pathogenesis n

n

n

n

The Ixodes species of tick has a four-stage, 2-year life cycle, which includes the egg, larval, nymphal, and adult stages. The host of the nymph and larval stages is the whitefooted mouse, which acts as a reservoir for the spirochete allowing for transmission to the tick. When the infected adult tick falls off the deer and attaches to the human host, it takes 24 hours for the spirochete to mobilize to the salivary glands of the tick and infect the host. It is thought that the spirochete remains in the body during the disease progression.

Risk Factors n n

Chronic arthritis associated with Lyme disease is more common with histocompatibility type DR4 Outdoor activities

Clinical Features n

n n n

Early disease is associated with erythema migrans at the site of the tick bite referred to as a target lesion. Local lymphadenopathy Flulike symptoms Cardiac manifestations such as various degrees of heart block may occur within 7 months.

190

n

Neurologic manifestations such as lymphocytic meningitis, radiculitis, polyneuropathy, cranial nerve palsies, and encephalopathy may occur within weeks to 12 months. Polyarthritis may last from 4 days to 2 years. The most commonly affected joints are the knee, shoulder, hip, elbow, ankle, wrist, and temporomandibular. Up to 32% of patients report back and neck pain. Late disease manifestations include persistent skin infection called acrodermatis chronica atrophicans; progressive encephalomyelitis; late polyneuropathy; and articular arthritis.

Natural History n

n

The initial stage is characterized by a general malaise similar to a flulike illness with neck and lower back pain associated with a characteristic erythema migrans. The later stage includes cardiac and neurologic symptoms such as polyradiculitis, arthritis, chronic fatigue, and encephalomyelitis.

Diagnosis Differential diagnosis Babesiosis n Ehrlichiosis n Radiculopathy n

History n Outdoor recreation n Tick bite n Flu-like symptoms n Myalgias, arthralgias n Skin rash Exam Erythema migrans n Regional lymphadenopathy n Musculoskeletal complaints are constant, irrespective of activity. n Irregular pulse with cardiac manifestations n Neurologic abnormalities include radiculitis, neurologic deficits, cranial nerve dysfunction, and impaired cognition. n Late disease manifestations include skin atrophy, persistent arthritis, cognitive deficits, and spastic paresis. n

Lyme Disease

Testing Elevated erythrocyte sedimentation rate n CSF may demonstrate increased protein concentration, lymphocytic pleocytosis, and antibodies to B. burgdorferi. n Synovial fluid analysis from an affected joint demonstrates an inflammatory arthropathy. n The enzyme-linked immunosorbent assay (ELISA) test, confirmed by Western blot analysis can be used to detect the presence of antibodies. n X-rays may demonstrate loss of articular cartilage, osseous erosions, or chondrocalcinosis. n MRI may demonstrate scattered white lesions similar to other demyelinating diseases. n


n

191

Exercises n Gentle strengthening and stretching exercises Modalities n Heat, cold, ultrasound, and transcutaneous electrical nerve stimulation have been used for symptomatic relief of pain and muscle spasms. Injection Possible joint fluid aspiration to rule out a septic joint

n

Surgical n None Consults n Infectious disease n Rheumatology Complications of treatment n Progressive disease due to incomplete treatment

Red Flags Progressive neurologic changes

Prognosis n

Treatment Medical n Children and pregnant females are treated with amoxicillin. n Early stage treated with doxycycline or tetracycline n Erythromycin is used with penicillin allergy. n Antibiotics for 14 to 21 days n In the late stage, intravenous antibiotics for 14 to 28 days are given, although the treatment response may be delayed up to 6 to 8 months.

n n

Excellent prognosis if identified early and treated with antibiotics. Radiculopathy and neuropathies may resolve in 24 months. Poor prognosis with neurologic deficits

Helpful Hints n

Proper dress during late spring to late summer

Suggested Reading Feder HM Jr, Johnson BJ, O’Connell S, et al. A critical appraisal of “chronic Lyme disease.” N Engl J Med. 2007;357(14):1422–1430.


n

Peripheral Neuropathy Description

n

Peripheral neuropathy indicates damage to the peripheral nerve. Symptoms generally include weakness, numbness, burning pain, and loss of reflexes.

n n

Etiology/Types n n n n n n n n

Demyelinating neuropathies Focal and multifocal neuropathies Motor and sensory neuropathies Small fiber and autonomic neuropathies Chronic axonal neuropathies Inheritable neuropathies Guillain-Barré syndrome (GBS) Chronic inflammatory demyelinating polyradiculopathy (CIDP)

Epidemiology n n

2% to 8% prevalence of neuropathy that increases with age Diabetes mellitus: most commonly presenting as distal symmetric sensorimotor neuropathy

Pathogenesis n n n

Damage to the axon results in wallerian degeneration, which leaves the surrounding stroma intact. Neuronopathies result in damage proximally at the dorsal root ganglion and/or motor root. Myelinopathies result in damage to the myelin sheath.


Diabetes mellitus is most common. Environmental exposures to solvents, acrylamide, and arsenic Hereditary factors Medications include amiodarone, statins, phenytoin, chemotherapy, and antibiotics.


n

The initial presentation usually includes pain, weakness, altered sensation, or autonomic symptoms. Advanced changes include distal muscle wasting and weakness, sensory loss in a glove-and-stocking distribution, and loss of deep tendon reflexes. Neuropathies marked by wallerian degeneration exhibit symmetric length-dependent changes affecting the feet followed by the hands.

192

n n n

Mononeuropathies are usually due to thyroid disease, occupation, pregnancy, or amyloidosis. Vasculitic mononeuropathies can occur over 24 to 72 hours Focal symptoms may allow for the identification of the individual affected nerve or root. Demyelinating neuropathies usually affect the longer fibers. Dorsal root ganglionopathies present with multisegmental sensory changes Small fiber dysfunction results in autonomic symptoms, loss of temperature, and pain.

Natural History n

Variable

Diagnosis Differential diagnosis Cervical spondylotic myelopathy (elderly) n Chemicals: solvents, acrylamide, and arsenic n Myelopathy n Pharmaceuticals: amiodarone, statins, phenytoin, chemotherapy, and antibiotics n Recreational drugs include tobacco, alcohol, and cocaine. n Spinal cord injury n Spinocerebellar syndromes n Transverse myelitis n Vitamin B deficiency 12 n

History Pins and needles sensation n Numbness n Burning sensation n Unsteadiness or stumbling n Weakness/difficulty with fine motor control n

Exam Facial weakness: GBS n Proximal motor weakness: GBS, CIDP n Loss of distal reflexes: length-dependent axonopathies n Generalized loss of reflexes: acquired demyelinating neuropathies n Sensory testing should test large fiber (proprioception and vibration) as well as small fiber (pain, temperature and pinprick). n

Peripheral Neuropathy

Small-fiber involvement assessed via papillary light reflex and standing and supine postural blood pressure measurements.

Testing n Preliminary laboratory testing should include a complete blood count, fasting blood glucose levels, glucose tolerance test, renal function tests, liver function tests, thyroid function, Vitamin B12, folate, paraprotein screen, vasculitis screen, and erythrocyte sedimentation rate. n Electrodiagnostic studies n Nerve biopsy considered with the possibility of a systemic disorder n CSF analysis can be used to determine if the CSF protein is elevated with cases of CIDP. n Anti-GM1 and anti-GD1a antibodies are found in GBS. Pitfalls n Carcinoma of the prostate n Hypokalemia n Arteriovenous malformation n Tumor of the conus medullaris n Difficult differentiating residual deficits from a chronic process

n n n

Exercises n Generalized strengthening and stretching Modalities Heat, cold, ultrasound, and transcutaneous electrical nerve stimulation have been used for symptomatic relief of pain and muscle spasms.

n

Injection None

n

Surgical None

n

Consults n Physical medicine and rehabilitation n Neurology Complications of treatment Variable

n

Prognosis n

Red Flags n n n

Transverse myelitis Arteriovenous malformation Tumor of the conus medullaris

B12 replacement CIDP: corticosteroids, intravenous immunoglobulin, plasma exchange Neuropathic pain: gabapentin, anticonvulsants, tricyclic antidepressants, and tramadol

Variable, can result in severe morbidity and mortality

Helpful Hints n

About 20% of neuropathies remain undiagnosed.

Treatment

Suggested Reading

Medical n Diabetes management

Richardson JK. The clinical identification of peripheral neuropathy among older persons. Arch Phys Med Rehabil. 2002;83(11):1553–1558.


n

193

Piriformis Syndrome (Pseudosciatica) Description

Clinical Features

Piriformis syndrome is sciatica-like pain due to impingement of the sciatic nerve as it courses through the piriformis muscle.

n

Etiology/Types n

n

Primary piriformis syndrome describes all pathology related to the piriformis muscle, such as myofascial pain. Secondary piriformis syndrome is reserved for buttock pain with or without radiation down the lower extremity based on the location of the pathology in relation to the structures exiting the sciatic notch.

Epidemiology n n n

The incidence is thought to be 6% to 8% of all low back pain cases. Most often noted in the 30- to 40-year age group The female to male ratio is thought to be 3–6:1.

Pathogenesis n n

n

n n

The piriformis muscle is the largest of the short external rotators of the hip. Others external rotators of the hip include the superior and inferior gemellus, quadratus femoris, and obturator internus muscles. The piriformis muscle originates from the second to fourth sacral vertebrae, exiting the pelvis through the sciatic notch, and inserting on the upper portion of the greater trochanter. Variations are known to exist in the course of the sciatic nerve through the piriformis muscle. The exact mechanism of sciatica remains unknown, although theories include nerve entrapment due to adhesions from an initial injury such as a fall, compression due to myofascial pain, or compression of the nerve by the muscle or tendon with hip internal rotation.


Activities that increase hip external rotation Blunt trauma to the gluteal region Pregnancy Prolonged sitting on hard surfaces

194

n n

Considered a diagnosis of exclusion No consensus on clinical findings “Sciaticalike” features

Natural History n

Progressive limp may overload adjacent structures

Diagnosis Differential diagnosis n Endometriosis n Herniated nucleus pulposus n Hip joint pathology n Pelvic tumors n Sacroiliac joint pathology n Spinal stenosis n Spondylosis History Sitting intolerance n Buttock pain with or without radiation into the posterior lower extremity n Pain improves with recumbency and worsens with activity. n

Exam A limp may develop in the affected side. n The straight leg raise sign may be positive. n Pace test increases pain with resisted leg abduction in a sitting position. n Beatty test places the patient in a side-lying position with the painful side up, the painful leg flexed with the knee resting on the table. Buttock pain develops when the patient holds the knee off the table. n Freiberg test forcefully rotates the extended thigh internally to elicit buttock pain by stretching the piriformis muscle. n FADIR test: buttock pain with hip flexion, adduction, and internal rotation n Palpation may note a characteristic tender palpable mass within the piriformis muscle or the sciatic notch. n

Testing Bone scan may note an increased uptake. n Muscle enlargement may be found on MRI or CT. n Nerve conduction testing demonstrates conduction delays in F waves and H reflexes. n

Piriformis Syndrome

n

EMG testing may demonstrate denervation potentials below the piriformis muscle. FADIR positioning has been shown to delay the H reflex.

Pitfalls n Missed diagnosis

Red Flags n

Other sacroiliac or hip joint pathology

Treatment Medical n NSAIDs n Analgesics n Muscle relaxants Exercises n Piriformis muscle stretching with internal rotation, hip adduction, and flexion n Thiele’s massage (transrectal massage)

n n

Surgical n Surgical release of the piriformis muscle results in only a minor change in strength in the external rotators and abductors of the hip. Consults Physical medicine and rehabilitation n General surgery n

Complications of treatment n Progressive limp may overload adjacent structures n Nerve injury related to injections

Prognosis n

Injection n Trigger point injections for symptoms of myofascial pain n Perisciatic corticosteroid injection

Generally assumed to be good, although small case series have reported good results with surgical release

Helpful Hints n


Caudal epidural steroid injection for radicular symptoms Botulinum toxin injection

The history and physical examination allow the practitioner to exclude other causes in the differential diagnosis.

Suggested Readings Fishman LM, Dombi GW, Michaelsen C, et al. Piriformis syndrome: diagnosis, treatment, and outcome, a 10-year study. Arch Phys Med Rehabil. 2002;83(3):295–301. Papadopoulos EC, Khan SN. Piriformis syndrome and low back pain: a new classification and review of the literature. Orthop Clin North Am. 2004;35(1):65–67.


n

195

Polymyalgia Rheumatica Description

n

Polymyalgia rheumatica is a clinical syndrome characterized by severe pain and tenderness in the proximal musculature of the extremities.

n n n n

Etiology/Types n

Unknown

n n n

Epidemiology n n n

Incidence is generally 11 per 100,000 individuals. Incidence is 50 to 100 cases per 100,000 people in individuals ≥50 years old Male to female ratio is 1:4.

Pathogenesis n n

Thought to be an arthritic condition affecting the axial joints. Possible immunologic and viral causes

n

Giant cell arteritis Malignancy Myofascial pain syndrome Osteoarthritis Polymyositis Rheumatoid arthritis Subacute bacterial endocarditis Thyroid or parathyroid dysfunction Viral infection

History n Females over 50 years of age n History of recent illness n Pain that is worse in the morning or with inactivity and pain improved with activity n Diffuse ache in the neck, shoulders, lower back, and pelvic girdle Exam Characteristic muscle tenderness to palpation and activity n Pain-limited joint active range of motion n Full-joint passive range of motion n Possible peripheral asymmetrical arthritis n

Risk Factors n

Unknown

Clinical Features n

n n n n n n n

Diagnostic criteria include age over 50 years; bilateral neck, shoulder, or pelvic girdle pain; more than 1 hour of morning stiffness; erythrocyte sedimentation rate >40 mm/h; a rapid response to prednisone; and an exclusion of other diagnoses Classically found in females over 50 years of age having symmetric neck and shoulder pain and stiffness Sternoclavicular and the humeroscapular joints are the most commonly affected joints. 70% to 90% describe neck and shoulder pain. 50% to 70% describe lower back, pelvic, and thigh pain. Pain usually starts in the neck and shoulders and is worse in the morning or with inactivity. Constitutional symptoms may be present, such as fever and malaise A history of a recent illness may also be noted.

Natural History n

Usually a benign course that may last from 2 to 4 years

Diagnosis Differential diagnosis Fibromyalgia

n

196

Testing Elevated erythrocyte sedimentation rate n Occasionally there may also be hypochromic anemia and increased alkaline phosphatase n Muscle biopsy specimens are normal. n X-rays are usually unremarkable. n Bone scan may demonstrate increased uptake in the shoulder joints. n MRI may demonstrate subacromial or subdeltoid bursitis as well as synovitis of the hip. n


n

Red Flags n

None

Treatment Medical Daily oral corticosteroids usually improve symptoms within 24 to 48 hours. n Dose is titrated downward as the patient remains stable. n

Polymyalgia Rheumatica

NSAIDs may be helpful in pain control for patients with mild disease

Exercises General conditioning exercises and range of motion stretching

n

Modalities n Heat, cold, ultrasound, and transcutaneous electrical nerve stimulation have been used for symptomatic relief of pain and muscle spasms. Injection Intramuscular methylprednisolone every 3 to 4 weeks has been shown to control symptoms. n Trigger point injections for symptoms of myofascial pain n

Surgical None

n

Consults Rheumatology n Physical medicine and rehabilitation n

Complications of treatment n Related to prolonged corticosteroid use including osteoporosis and immune suppression

Prognosis n n n

There is a 30% relapse rate for patients who discontinue oral corticosteroids before 2 years. Corticosteroid therapy may continue for 57 years. The course of the disease usually lasts from 2 to 4 years.

Helpful Hints n n

Need to exclude other diagnoses Benign course

Suggested Readings Nothnagl T, Leeb BF. Diagnosis, differential diagnosis and treatment of polymyalgia rheumatica. Drugs Aging. 2006;23(5):391–402. Soubrier M, Dubost JJ, Ristori JM. Polymyalgia rheumatica: diagnosis and treatment. J Bone Spine. 2006;73(6):599–605.


n

197

Psychological/Psychiatric Issues Description Psychological barriers to pain resolution

Etiology/Types n

n

n

n

n

Somatoform disorders include conversion disorder, somatization disorder, body dismorphic disorder, hypochondriasis, and pain disorder. Psychogenic rheumatism includes musculoskeletal complaints in the absence of organic disease and a diagnosed psychiatric illness. Camptocormia describes a condition where, following a trivial injury, the individual is bent forward with arms hanging loosely with a downward gaze. Common in industrial workers and soldiers Conversion disorder is a syndrome affecting the voluntary nervous system that contraindicates normal musculoskeletal and neurologic physiology, Malingering is a conscious misrepresentation of signs and symptoms for secondary gain,


22% to 66% of psychiatric patients report pain. 25% of psychiatric patients report severe pain. Lower back is the most common site of pain. Other sites of pain include the head, neck, chest, flank, pelvis, and the entire body. Malingering is most common in the workplace and is associated with workers’ compensation. Fewer than 5% of patients with back pain are thought to be malingerers.

Diagnosis Differential diagnosis Organic versus nonorganic illnesses

n

History Pain drawings demonstrate large areas of pain n Difficulty with tasks associated with mobility and activities of daily living n

Exam Conversion disorder demonstrates an inconsistent exam. n Malingering patients may refuse to participate in components of the exam. n Normal lumbar or cervical lordosis with no paraspinal muscle spasm is unlikely in a patient with a history of chronic pain. n Variable tenderness to palpation during the exam n Intense pain and withdrawal with light palpation n Hoover’s test is done with the patient supine. The examiner places both hands underneath the patient’s heels and then asks the patient to raise one leg. Normally, there should be downward pressure on the contralateral heel; if no pressure is noted then malingering may be suspected. n Cog-wheel rigidity or sudden give-way weakness n Hyperactive deep tendon reflexes n Waddell signs include diffuse nonspecific tenderness, overreaction, regionalization, distraction, and stimulation. n

Testing Imaging studies may be used to rule out significant pathology n Electrodiagnostic studies may help to differentiate pathology. n

Pathogenesis n

Possibly related to increased anxiety, hysteria, muscle tension, and hallucination

Risk Factors n

Risk factors for conversion disorders include young females with limited education, low income, and difficulty expressing distress.


Very difficult to differentiate Conversion disorder includes loss of extremity function or bowel or bladder dysfunction.

Pitfalls n Overlooked organic illness

Red Flags n n

Treatment Medical Psychiatric medications consistent with the psychiatric diagnosis n Psychotherapy n

Natural History n

Variable

198

Neurologic deficits Suicidal ideations

Psychological/Psychiatric Issues

Exercises Sequential exercise regimens have been used to overcome patient’s fear, avoidance, or conversion disorder and return the patient to normal function. n It may be difficult to convince a patient to participate in an exercise program. n


n

Injection n None Surgical n None Consults Psychiatry n Psychology n Physical medicine and rehabilitation n Referral to another physician for a second unbiased opinion n

Complications of treatment Variable

199

Prognosis n

n n

60% of conversion disorders may improve within 2 weeks; 98% will improve in one year with identification of underlying stress and normal findings 25% of conversion disorder patients have recurrence within the first year. Some patients with spinal pain may not improve.

Helpful Hints n

Always be alert for a possible organic illness

Suggested Readings Letonoff EJ, Williams TR, Sidhu KS. Hysterical paralysis: a report of three cases and a review of the literature. Spine. 2002;27(20):E441–E445. McDermott BE, Feldman MD. Malingering in the medical setting. Psychiatr Clin North Am. 2007;30(4):645–662. Rashbaum IG, Sarno JE. Psychosomatic concepts in chronic pain. Arch Phys Med Rehabil. 2003;84(3 suppl 1): S76–S80. Trieschmann RB, Stolov WC, Montgomery ED. An approach to the treatment of abnormal ambulation resulting from conversion reaction. Arch Phys Med Rehabil. 1970;51(4):198–206. Section II: Spine-Mimicking Conditions

n

Shoulder Impingement Syndrome Description

develops into full thickness tears, tendon ruptures, and bony changes.

Shoulder impingement syndrome is the most common disorder of the shoulder.

Diagnosis Etiology/Types n

Subacromial bursitis, partial rotator cuff tears, rotator cuff tendinosis, and calcified tendonitis

Epidemiology n n

Incidence of shoulder pathology ranges from 7 to 25 per 1,000 visits to primary care physicians. Prevalence ranges from 7% to 27% in those 70 years of age.

Pathogenesis n

Repetitive or excessive contact or abrasion of the rotator cuff muscles and/or tendons due to compression between the humeral head and acromion, coracoacromial ligament, and acromioclavicular joint.


Deconditioning Neurologic injuries Sports involving throwing or overhead activities Trauma

Clinical Features n

n n n

n

Shoulder pain causes pain along the scapula and trapezius muscle, but not the neck; pain worsens with forward flexion of the shoulder; pain is often referred to the lateral shoulder and mid-arm. Patients note difficultly in removing a shirt or coat. Cervical pathology can radiate into the shoulder and shoulder pathology can radiate into the neck. Cervical pathology may lead to secondary shoulder disease, such as frozen shoulder. Atrophy of the shoulder musculature can be associated with either C5 or C6 radiculopathy or chronic rotator cuff injury. Active shoulder range of motion limitations may be related to deltoid or rotator cuff weakness, resulting from a cervical radiculopathy or disuse atrophy caused by pain.

Natural History n

Progresses from edema and hemorrhage to cuff fibrosis and thickening or a partial cuff tear and finally

200

Differential diagnosis Cervical disc herniation with radiculopathy n Cervical myelopathy n Cervical spondylosis n Frozen shoulder n Glenohumeral instability or osteoarthritis n Lung tumors n Nerve palsies n Shoulder impingement syndrome n

History Pain with shoulder range of motion n Difficulty or pain with putting on shirts or coats n Difficulty or pain with overhead activities n Pain at night n Pain located deep in the shoulder or in the lateral proximal arm n

Exam Inspection of muscle tone, symmetry, and deformity n Palpation to assess for areas of swelling, tenderness or other abnormalities n Active and passive neck and shoulder range of motion n Strength testing of the upper extremities n Biceps, triceps, and brachioradialis reflex testing n Sensation testing of the upper extremities n Neer’s and Hawkin’s impingement signs n Resisted abduction of the arm tests strength and may also reproduce pain n The best combination for subacromial impingement syndrome are the Hawkins sign, external rotation weakness, and horizontal abduction n

Testing X-rays of the shoulder should include anterior– posterior, lateral, and axillary views n MRI is the study of choice for assessing for rotator cuff tears. n MRI may detect rotator cuff tears in 34% of asymptomatic individuals and this frequency increases with age n CT is useful in diagnosing subtle dislocations, labral tears, full thickness rotator cuff tears, bony lesions, or subtle dislocation. n

Shoulder Impingement Syndrome n n

Musculoskeletal ultrasonography Electrodiagnostic studies are useful in differentiating shoulder pathology from radiculopathy and myopathy as well as determining the severity and chronicity of the neurologic process.

Pitfalls n MRI findings may not correlate with the patient’s symptoms

n

n n

201

Intra-articular or subacromial corticosteroid and anesthetic injections have been shown to provide short-term relief. Intra-articular sodium hyaluronates into the glenohumeral joint or bursa have been well tolerated. Intra-articular injections should be done under imaging guidance, if available.

Surgical Open acromioplasty and rotator cuff repair in 21 patients with electrodiagnostically documented cervical radiculopathy has demonstrated decreased shoulder pain in 87% of patients and decreased neck pain in 66% of patients.

n n n n

Joint infection Fracture Glenohumeral dislocation

Treatment Medical n Rest n Ice n NSAIDs n Acetaminophen Exercises n Progressive strengthening exercises of the rotator cuff muscles Modalities Heat, cold, ultrasound, and transcutaneous electrical nerve stimulation have been used for symptomatic relief of pain and muscle spasms.

n

Injection Anesthetic injection into the subacromial region can help with diagnosis and treatment.

n

Consults Physical medicine and rehabilitation n Orthopedic surgery n


Prognosis n n

Progression of a partial rotator cuff tear to a full tear with loss of shoulder function Mobility may be maintained even with evidence of a full rotator cuff tear.

Helpful Hints n

Emphasis on strengthening and stretching

Suggested Reading Hawkins RJ, Bilco T, Bonutti P. Cervical spine and shoulder pain. Clin Orthop Relat Res. 1990;(258):142–146.


Red Flags

Trochanteric Bursitis Description

n

Trochanteric bursitis is a regional pain syndrome described as an aching intermittent pain over the lateral hip region.

n

Etiology/Types

n

Total hip arthroplasty Trauma is noted in up to 64% of patients.

Clinical Features n

Acute, subacute, and chronic types n


One of the most common causes of hip pain Incidence is 1.8 to 5.6 per 1,000 adults in 1 year Most common in the 40- to 60-year-old age group, but found in all age groups Female to male ratio is of 2–4:1.

Pathogenesis Gluteus minimus bursa lies slightly anterior and above the proximal superior surface of the greater trochanter. n Subgluteus medius bursa lies underneath the gluteus medius muscle and is located supraposteriorly of the proximal edge of the greater trochanter. n Subgluteus maximus bursa is 4 to 6 cm long and 24 cm wide and located lateral to the greater trochanter at the convergence of the tensor fascia lata and gluteus maximus, as they form the iliotibial tract. – Allows the anterior part of the gluteus maximus tendon to pass over the trochanter to insert into the iliotibial band. – Irritation results in trochanteric bursitis.

n n n n

n

Risk Factors n n n n n n n n n n n n n

Biomechanical alterations in the lower extremity such as lower-extremity joint osteoarthritis Tendinous calcification Deconditioning Degenerative hip changes Hemiparesis Iliotibial band syndrome Leg-length discrepancy Lumbar spondylosis Obesity Pes planus Radiculopathy Repetitive microtrauma Residual weakness following spine or hip surgery

202

n

Acute, subacute, or chronic intermittent sharp or aching pain on the lateral hip Radiation into the lateral thigh occurs in 25% to 40% of cases. Maximal tenderness is often at the junction of the upper thigh and greater trochanter. Maximal tenderness can be located just posterior to the apex of the greater trochanter. Most often worsened with active hip external rotation and abduction Occasionally worsens with active internal rotation or extension of the hip Worsens with prolonged standing, prolonged walking, running, and ascending or descending stairs

Natural History n n n n

May lead to calcification in the region of the greater trochanter May lead to significant disability May last months to years Some clinicians believe it is a self-limiting disease.

Diagnosis Differential diagnosis Acetabular labral tear n Avascular necrosis n Femoral neck stress fracture n Gluteus minimus and medius tears or tendonitis n Hip osteoarthritis n Lumbar compression fractures n Lumbar spine degenerative changes n Lumbar radiculopathy n

History Waxing and waning pain n Lateral hip pain that radiates down the lateral thigh but rarely to the knee or below. n Worsens with climbing stairs, sleeping on the ipsilateral side, or at night in general n

Exam Palpation of the greater trochanter at the insertion of the gluteus medius muscle

n

Trochanteric Bursitis n n

“Jump” sign at the site of maximal tenderness on the greater trochanter Positive FABER test

Testing X-rays may demonstrate calcifications in the region of the greater trochanter and an irregular surface of the greater trochanter n MRI may demonstrate increased signal on short tau inversion recovery sequences and distension of the greater trochanteric bursa. n Bone scan may demonstrate increased uptake in the region of the greater trochanter n Musculoskeletal ultrasound may demonstrate enlargement of the subgluteus maximus bursa, deep trochanteric bursa of the gluteus medius, and minimus. n

Pitfalls Trochanteric bursitis is found in 18% to 45% of patients who present with low back pain. n Pseudoradiculopathy that presents with radiation of pain along the iliotibial tract mimics nerve root irritation. n

203

Modalities n Heat, cold, ultrasound, and transcutaneous electrical nerve stimulation have been used for symptomatic relief of pain and muscle spasms. Injection Blind corticosteroid and anesthetic injections at the site of maximal tenderness with surrounding infiltration n Musculoskeletal ultrasound and fluoroscopic guidance have been used to more accurately target the bursae with improved outcomes. n

Surgical Considered in refractory cases n Considered for excision of the calcifications, bursal sac, and iliotibial band release with good results in small case series n

Consults Physical medicine and rehabilitation n Orthopedic surgery n


Hip fracture

Treatment Medical Behavior modification n Weight loss n NSAIDs n Contralateral heel lift for leg-length discrepancy n Use of a cane n

Exercises n Hip and lower back strengthening and stretching

Prognosis n

Depending on the underlying etiology may last for years

Helpful Hints n

Trochanteric bursitis may be a primary or secondary diagnosis in patients with low back pain

Suggested Reading Shbeeb MI, Matteson EL.Trochanteric bursitis (greater trochanter pain syndrome). Mayo Clin Proc. 1996;71(6):565–569.


Red Flags n


Index Achondroplasia, 2–3 Aging lumbosacral spine, 4–5 Allen Ferguson scale, 72 Aneurysmal bone cysts, 6–7 Angiography, 83 Ankylosing spondylitis, 8–9 Anterior cord syndrome, 10–11 Anterior spinal artery syndrome; see anterior cord syndrome Arachnoiditis, 12–13 Arteriovenous malformation, 14–15 Atlantoaxial instability (AAI), 16–17 Atlantoaxial subluxation, 74 Atlantodens interval (ADI), 16 Atlanto-occipital dislocations, 74 Atlas fractures, 74, 75 Aviation-associated back and neck pain, 18–19 Baastrup’s disease, 20–21 Back pain associated with dance, 22–23 associated with golf, 24–25 associated with heavy loads, 26–27 associated with occupation, 28–29 associated with pregnancy, 30–31 associated with sitting, 32–33 associated with soccer, 34–35 associated with tennis, 36–37 aviation associated, 18–19 in mature athletes, 38–39 in older population, 40–41 in young athletes, 42–43 Bamboo spine, 9 Borrelia burgdorferi, 190 Brown-Séquard syndrome, 44–45 Burst fractures, 76, 77 Camptocormia, 198 Carpal tunnel syndrome, 180–181 Cauda equina syndrome, 46–47 Central cord syndrome, 48–49 Chondrosarcoma, 50–51 Chordoma, 52–53 Coccydynia, 54–55 Coccygodynia; see coccydynia Complex regional pain syndrome, 182–183 Compression extension injuries, 72 Compression fractures, 77 Compression–flexion injuries, 72

205

Conversion disorder, 198 Coxsackievirus, 96 Cumulative trauma disorder (CTD), 104 Curettage, 81 Deconditioning, 56–57 Diffuse idiopathic skeletal hyperostosis (DISH), 58–59 Disciitis, 60–61 Distraction extension injuries, 72 Distractive flexion injuries, 72 Echovirus, 96 Ehlers–Danlos syndrome (EDS), 62–63 Embolization, 81 En bloc excision, 81 En bloc spondylectomy, 68 Epidural abscess, 64–65 Epidural lipomatosis, 66–67 Escherichia coli, 96 Ewing’s sarcoma, 68–69 Failed back surgery syndrome, 70–71 Fibromyalgia, 184–185 Flexion distraction injuries, 77 Forrestier’s disease; see diffuse idiopathic skeletal hyperostosis (DISH) Fractures of lower cervical spine, 72–73 of sacrum, 78–79 of thoracolumbar spine, 76–77 of upper cervical spine, 74–75 Giant cell tumor, 80–81 Gluteus minimus bursa, 202 Gravid uterus, 30 Haemophilus influenzae, 96 Hangman’s fracture, 74 Hemangiomas, 82–83 Hemoglobinopathies, 84–85 Herpes zoster, 186–187 Hip–spine syndrome (HSS), 188–189 Hyperparathyroidism, 86–87 Isolated Jefferson fractures, 75 Ixodes species, of tick, 190

206

Index

Kissing Spines disease; see Baastrup’s disease Klippel–Feil syndrome, 108 Laminectomy, 83 Lateral flexion injuries, 72 Long-term gait dysfunction, 79 Lordotic back pain, 42 Low back strain, 88–89 Lumbar disc herniation, 30 Lyme disease, 190–191 Lymphoma, 90–91 Marfan syndrome, 92–93 Meningioma, 94–95 Meningitis, 96–97 Multiple myeloma, 98–99 Multiple sclerosis, 100–101 Myelopathy, cervical; see spinal stenosis, cervical Myofascial pain syndrome, 102–103 Neck pain associated with occupation, 104–105 in athletes, 106–107 aviation-associated, 18–19 strain, 108–109 Neisseria meningitides, 96 Neurofibroma, 110–111 Occipital condyle fractures, 74, 75 Occupational cervicobrachial disorder (OCD), 104 Odontoid fracture, 74, 75 Osteoblastoma, 112–113 Osteochondroma, 114–115 Osteogenesis imperfecta, 116–117 Osteoid osteoma, 118–119 Osteomyelitis, vertebral, 120–121 Osteoporosis, 122–123 Paget’s disease, 124–125 Paraplegia, 146 Parathyroid hormone (PTH), 86 Percutaneous vertebral augmentation, 83 Peripheral neuropathy, 192–193 Piriformis syndrome, 194–195 Polymyalgia rheumatica, 196–197 Posterior atlantodental interval (PADI), 16 Postlaminectomy kyphosis, 69 Psoriatic arthritis, 126–127 Psychogenic rheumatism, 198 Psychological/psychiatric issues, 198–199

Radical excision, 81 Radiculopathy cervical, 128–129 lumbar, 132–133 thoracic, 130–131 Reflex sympathetic dystrophy; see complex regional pain syndrome Relaxin, 30 Repetitive strain injury (RSI), 104 Retrovirus, 96 Rheumatoid arthritis (RA), 134–135 Sacral stress fractures, 79 Sacroiliac joint pain, 136–137 Sarcoidosis, 138–139 Scheuermann’s disease, 140–141 Schmorl’s node, 4 Schwannoma, 142–143 Scoliosis, 144–145 Seating, reclined, 32 Shingles; see herpes zoster Shoulder impingement syndrome, 200–201 Sickle cell anemia, 84, 85 Sitting, prolonged, 32 Somatoform disorders, 198 Spinal cord compression, 83 Spinal cord injury, 146–147 acute, 83 Spinal instability, 83 Spinal stenosis cervical, 148–149 lumbar, 152–153 thoracic, 150–151 Spondylolysis/ spondylolisthesis, 42 cervical, 154–155 lumbar, 156–157 Spontaneous epidural hematoma, 158–159 Staphylococcus aureus, 96 Staphylococcus epidermidis, 96 Stingers and burners, 160–161 Streptococcus pneumoniae, 96 Subgluteus maximus bursa, 202 Subgluteus medius bursa, 202 Supine positioning, prolonged, 30 Synovial cysts, 162–163 Syringomyelia, 164–165 Tarlov cysts, 166–167 Temporomandibular dysfunction, 172 Tethered cord syndrome, 168–169 Tetraplegia, 146 Thalassemia, 84, 85 Thoracic myelopathy; see spinal stenosis, thoracic

Index

Thromboembolism, 77 Tissue deoxygenation, 84 Tissue tightness, 42 Transverse fractures, 79 Transverse myelitis, 170–171 Traumatic spondylolisthesis of the axis, 74 Trochanteric bursitisis, 202–203 Upper thoracic–compression fractures, 77 Varicella-zoster virus (VZV), 186

Vertebral fractures, 86 Vertical compression injuries, 72 Whiplash-associated disorders, 172–173 Worker’s compensation, 28–29 Work-related musculoskeletal disorder (WMSD), 104–105 Zygapophyseal (facet) joint pain cervical, 174–175 lumbar, 176–177

207

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